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accession_id stringlengths 10 10 | pmid stringlengths 1 8 | figure_idx int16 1 48 | figure_fn stringlengths 1 33 | figure image | caption stringlengths 0 6.52k | license stringclasses 3
values | retracted stringclasses 2
values | last_updated stringlengths 19 19 | citation stringlengths 25 85 |
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PMC1193645 | 14699080 | 1 | 20020509f1 | Figure 1. Spontaneous EAE development in wild-type and STAT1-deficient mice. (A) TCR + STAT1 −/− H-2 b/u mice and their TCR + STAT1 +/− H-2 b/u littermates (30 animals/group) were monitored for 6 mo and the spontaneous development of EAE (level 5) was recorded. (B) Same as in A, but TCR + STAT1 −/− H-2 u/u mic... | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 2 | 20020509f2 | Figure 2. Flow cytometric analysis of wild-type, asymptomatic, or paralyzed STAT1-deficient mice. (A) Cells derived from lymph nodes of wild-type, asymptomatic, or paralyzed STAT1-deficient animals were stained for CD4, CD69, and Vβ8. Horizontal axis represents Vβ8 staining, vertical axis corresponds to CD4 (top) or CD... | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 3 | 20020509f3 | Figure 3. Immunohistological analysis of CNS tissue from asymptomatic and paralyzed STAT1-deficient mice. Brains and spines were removed from asymptomatic or paralyzed (level 5) STAT1-deficient mice and fixed in formaldehyde. Paraffin-embedded sections were stained with hematoxylin and eosin. | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 4 | 20020509f4 | Figure 4. Proliferation of wild-type and STAT1-deficient CD4 + cells. (A) CD4 + cells were purified from the spleens of wild-type or STAT1-deficient mice as described in Materials and Methods, and proliferation was assessed by thymidine incorporation in response to stimulation with 1.0 μg/ml Con A in the presence of ... | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 5 | 20020509f5 | Figure 5. (A and B) Flow cytometric analysis of thymocytes in wild-type and STAT1-deficient mice. Cells derived from thymi of wild-type or STAT1-deficient animals were stained for CD4, CD8, and CD25. The ratio of CD4 + CD8 − CD25 + cells as the percentage of total CD4 + CD8 − cells is shown. | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 6 | 20020509f6ab | Figure 6. Effect of wild-type CD4 + CD25 + cells on the proliferation of STAT1 −/− CD4 + cells. (A) CD4 + cells were purified from the spleens of wild-type or STAT1-deficient mice as described in Materials and Methods. Wild-type or STAT1-deficient CD4 + cells were either incubated separately, mixed in a 1:1 ratio... | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1193645 | 14699080 | 7 | 20020509f7 | Figure 7. STAT1-deficient CD4 + CD25 + cells fail to suppress T cell proliferation. CD4 + CD25 + and CD4 + CD25 − cells were purified from spleens as described in Materials and Methods. Wild-type or STAT1-deficient CD4 + CD25 − cells were labeled with CFSE and their proliferation in response to 1.0 μg/ml Con A ... | CC BY-NC-SA | no | 2022-01-13 08:52:49 | J Exp Med. 2004 Jan 5; 199(1):25-34 | |
PMC1237012 | 15583013 | 1 | 20040915f1 | Figure 1. Restriction maps of CD73 genomic DNA, targeting vector, and recombined allele. (A) CD73 genomic DNA, including exon 3 and intronic sequences used to construct the short (1 kb) and long arms (4.2 kb) of the targeting vector. (B) CD73 targeting vector showing the antisense orientation of the CD73 sequences rela... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 2 | 20040915f2 | Figure 2. CD73 expression and function on leukocytes from Cd73
+/+ and Cd73
−/− mice. CD73 expression was evaluated on leukocytes from lymph node, spleen, peripheral blood, bone marrow, and thymus from Cd73
+/+ (left) and Cd73
−/− (right) mice with monoclonal antibody TY/23 + PE–goat anti–rat IgG. Stain... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 3 | 20040915f3 | Figure 3. Vascular leakage in Cd73 -deficient mice in vivo. Cd73
−/− mice (black bars) and age-, weight-, and gender-matched littermate controls (white bars) were administered intravenous Evan's blue (0.2 ml of 0.5% in PBS per mouse) and exposed to room temperature air (A) or normobaric hypoxia (B, 8% O 2 , 92% N ... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 4 | 20040915f4 | Figure 4. Influence of CD73 inhibition on vascular leakage in vivo. Age-, weight-, and gender-matched mice were administered APCP (20 mg/kg i.p.) or an equal volume of PBS followed by intravenous Evan's blue solution (0.2 ml of 0.5% in PBS per mouse) and exposed to room temperature air (A) or to normobaric hypoxia (B, ... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 5 | 20040915f5 | Figure 5. Vascular leakage and reconstitution of Cd73
−/− mice with 5′-NT. Cd73
−/− mice (B and D) and age-, weight-, and gender-matched littermate controls (A and C) were administered 5′-NT purified from C. atrox venom (500 U/kg i.p.; black bars) or PBS (white bars) followed by intravenous Evan's blue soluti... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 6 | 20040915f6 | Figure 6. Influence of adenosine receptor antagonists on hypoxia-induced vascular leakage. Wild-type mice were administered either PBS (Control), the A 2B receptor antagonist MRS1754 (1 mg/kg i.p. plus 1 mg/kg s.c.) or the A 2A receptor antagonist ZM241385 (1 mg/kg i.p. plus 1 mg/kg s.c.) followed by intravenous Evan... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 7 | 20040915f7 | Figure 7. Influence of the adenosine receptor agonist NECA on vascular leakage of Cd73
−/− mice. Cd73
−/− mice (B and D) and age-, weight-, and gender-matched littermate controls (A and C) were administered the adenosine analogue NECA (0.1 mg/kg i.p. plus 0.1 mg/kg s.c., black bars) or PBS (white bars) followed... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237012 | 15583013 | 8 | 20040915f8 | Figure 8. Characterization of lungs from Cd73
−/− mice. Wild-type (A and D) or Cd73
−/− (B and C) mice were subjected to normoxia (A and B) or hypoxia (C and D). Whole lungs were fixed with 10% formalin at total lung capacity, sectioned, and stained with hematoxylin and eosin. (A) A representative image of a wi... | CC BY-NC-SA | no | 2022-01-13 08:53:02 | J Exp Med. 2004 Dec 6; 200(11):1395-1405 | |
PMC1237122 | 15699070 | 1 | 20041577f1 | Figure 1. LN1 nonproductive allele structure. Configurations of wild type and LN1 nonproductive (ΔD) IgH loci are depicted together with proposed intermediates. Nucleotides inserted during the ΔD rearrangement are highlighted in italics and nucleotides that are lost in the process of rearrangement are shaded. The ΔD re... | CC BY-NC-SA | no | 2022-01-13 09:00:15 | J Exp Med. 2005 Feb 7; 201(3):341-348 | |
PMC1237122 | 15699070 | 2 | 20041577f2 | Figure 2. ΔD/ΔD mice generate all peripheral B cell subsets with a low rate of B cell production. Representative flow cytometric analyses of lymphocytes in spleen (A), bone marrow (B), and peritoneal cavity (C) of ΔD/ΔD and WT mice. Shown are cells in the “lymphocyte gate” unless additional gates are specified. Numbers... | CC BY-NC-SA | no | 2022-01-13 09:00:15 | J Exp Med. 2005 Feb 7; 201(3):341-348 | |
PMC1237122 | 15699070 | 3 | 20041577f3 | Figure 3. The ΔD allele cannot compete with the WT allele in either B cell generation or antibody production. FACS analysis of CD19-gated splenocytes from 5-mo-old ΔD/ΔD, (BALB/c × ΔD)F1, (BALB/c × C57BL/6)F1, C57BL/6, and BALB/c mice for the expression of IgM of a and b allotypes. The ΔD allele is of the b allot... | CC BY-NC-SA | no | 2022-01-13 09:00:15 | J Exp Med. 2005 Feb 7; 201(3):341-348 | |
PMC1237122 | 15699070 | 4 | 20041577f4 | Figure 4. Analysis of IgH V region joints derived from B cells in ΔD mice. (A) Alignment of joints amplified from the RNA of 2-wk-old ΔD/ΔD and ΔD/JHT mice. The joints are shown from the codon immediately 5′ of the second cystein (position 104) of the V H gene and extending to the conserved glycine of the J H region.... | CC BY-NC-SA | no | 2022-01-13 09:00:15 | J Exp Med. 2005 Feb 7; 201(3):341-348 | |
PMC1237122 | 15699070 | 5 | 20041577f5 | Figure 5. Absence of newly generated B cells expressing the ΔD allele in heterozygous mutant mice. Immature and mature B cells in the bone marrow of 10-mo-old (BALB/c × ΔD)F1 mice were compared with those of 5-mo-old (BALB/c × C57BL/6)F1, BALB/c, and C57BL/6 mice ( n = 2 for each group) for expression of either IgM a ... | CC BY-NC-SA | no | 2022-01-13 09:00:15 | J Exp Med. 2005 Feb 7; 201(3):341-348 | |
PMC1255917 | 11470818 | 1 | 0104043f1 | Figure 1.
Relative replication timing of DHFR and β -globin loci. (A) Asynchronously growing CHO cells were pulse labeled with BrdU and hybridized in situ with digoxigenin-labeled DHFR cosmid cSc26 and biotin-labeled β-globin phage λJHC2. Sites of hybridization were visualized with FITC-conjugated antidigoxigenin a... | CC BY-NC-SA | no | 2022-01-13 07:19:29 | J Cell Biol. 2001 Jul 23; 154(2):283-292 | |
PMC1255917 | 11470818 | 2 | 0104043f2 | Figure 2.
The CHO β -globin locus is replicated during the stage of peripheral DNA synthesis. (A) Examples of early (type I/II), middle (type III), and late (type and type V) replication patterns, revealed by pulse labeling CHO AA8 cells with BrdU and staining with fluorescent anti-BrdU antibodies. (Top) Shows cell... | CC BY-NC-SA | no | 2022-01-13 07:19:29 | J Cell Biol. 2001 Jul 23; 154(2):283-292 | |
PMC1255917 | 11470818 | 3 | 0104043f3 | Figure 3.
Colocalization of β -globin versus DHFR doublets with sites of DNA synthesis during middle to late S phase. CHO AA8 cells pulse labeled with BrdU were subjected to FISH with either a β-globin or a DHFR probe (red) and then stained with anti-BrdU antibodies (green). Analysis was concentrated on nuclei that... | CC BY-NC-SA | no | 2022-01-13 07:19:29 | J Cell Biol. 2001 Jul 23; 154(2):283-292 | |
PMC1255917 | 11470818 | 4 | 0104043f4 | Figure 4.
Late replication of the β -globin gene locus in CHO cells is established 1–2 h after mitosis. (A) CHO AA8 cells were synchronized in mitosis and released into G1 phase. At the indicated times thereafter, cells were pulse labeled with BrdU, stained with anti-BrdU antibodies, and the percentage of BrdU posi... | CC BY-NC-SA | no | 2022-01-13 07:19:29 | J Cell Biol. 2001 Jul 23; 154(2):283-292 | |
PMC1255917 | 11470818 | 5 | 0104043f5 | Figure 5.
The repositioning of type III sequences and the peripheral localization of the β -globin locus are completed 1–2 h after mitosis. (A) Asynchronous cultures of CHO AA8 cells were pulse labeled with BrdU for 30 min. Metaphase cells were harvested 3.5 h thereafter, creating populations of cells in which late... | CC BY-NC-SA | no | 2022-01-13 07:19:29 | J Cell Biol. 2001 Jul 23; 154(2):283-292 | |
PMC1255922 | 11535615 | 1 | 0104099f1 | Figure 1.
Chk1 and Chk2 activation in response to HU and IR. (A) HeLa cell lysate (50 μg) subjected to SDS-PAGE and immunoblotted with anti-Chk1 antibodies. (B) Kinase assays in the presence of indicated concentrations of UCN-01 performed on Chk1 IPs from HeLa cell lysates. (C) HeLa cells ± caffeine (5 mM), were tre... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 2 | 0104099f2 | Figure 2.
S phase activation of Chk1 and Chk2 is independent of ATM. (A–D) ATM-null (AT221JE-T) cells were untreated, treated with HU (+HU, 2 mM) or irradiated (10 Gy, +IR) as indicated. (A) Cells were lysed, and kinase assays performed on Chk1 IPs. (B) Lysates subjected to SDS-PAGE and immunoblotted for Chk1. (C) K... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 3 | 0104099f3ad | Figure 3.
Activation of Chk1 and Chk2 requires DNA replication arrest. Metaphase HeLa cells collected by nocodazole treatment and mitotic shake-off were released into fresh medium +/−HU. 0.5 h before harvest, at indicated times after nocodazole release, cells were pulse labeled with BrdU, and aliquots removed for fl... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 4 | 0104099f4ab | Figure 4.
Differential inactivation of Chk1 and Chk2 following release from replication block. (A) Asynchronously growing HeLa cells were treated or not for 24 h with 2 mM HU or 5 μg/ml aphidicolin and lysates prepared. Kinase assays were performed on immunoprecipitated Chk1 and Chk2 (upper panels) as indicated. Lys... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 5 | 0104099f5 | Figure 5.
UCN-01 blocks Chk1 autophosphorylation in vitro and Chk1 hyperphosphorylation in vivo, with no effect on ATR kinase in vitro or S phase activation of Chk2 in vivo. (A) Chk1 autophosphorylation was measured by incorporation of 32 P from labeled ATP in the presence of 0 (lane 1), 10 nM (lane 2) 50 nM (lane ... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 6 | 0104099f6 | Figure 6.
UCN-01 inhibits replication checkpoint controlling replicon firing. (A) Asynchronous CHOC cells were pulse labeled with CldU and then treated with aphidicolin for 12 h either in the absence (extreme left-hand panels, +Aphidicolin) or in the presence of 300 nM UCN-01. At time points after aphidicolin additi... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255922 | 11535615 | 7 | 0104099f7 | Figure 7.
UCN-01 does not affect the timing of normal S phase progression. Three asynchronous CHOC cell cultures were pulse labeled for 10 min with CldU. Two of these were then chased +/−UCN-01. A third culture was incubated in parallel in the presence of aphidicolin and UCN-01. At indicated times after CldU labelin... | CC BY-NC-SA | no | 2022-01-13 07:19:32 | J Cell Biol. 2001 Sep 3; 154(5):913-924 | |
PMC1255929 | 12707307 | 1 | 200211127f1 | Figure 1.
Colocalization of origins used in two consecutive cell cycles. (A) Cells were synchronized at the G1/S border with aphidicolin, released for 10 min, and then pulse labeled with CldU for 10–60 min. Labeled cells were then synchronized in mitosis and blocked at the following G1/S. Aliquots were then released... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1255929 | 12707307 | 2 | 200211127f2 | Figure 2.
Colocalization of origins selected for initiation in vitro with those selected in vivo. (A) CHOC 400 cells were synchronized at the G1/S border with aphidicolin and then released from the aphidicolin block for 10 min. Cells were then pulse labeled with BrdU for 20–30 min and synchronized in mitosis. At 1 (... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1255929 | 12707307 | 3 | 200211127f3 | Figure 3.
Interorigin distances in vitro. (A) Intact nuclei from cells synchronized at 1, 2, or 5.5 h after mitosis were introduced into Xenopus egg extract supplemented with biotin-dUTP for 30–40 min. Digoxigenin-dUTP was then added, and reactions were incubated for an additional 2 h. (B) Shown are three exemplar... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1255929 | 12707307 | 4 | 200211127f4 | Figure 4.
Interorigin distances in vivo. Cells were synchronized at the G1/S border with aphidicolin, and the earliest replicating origins were labeled with IdU as in the legends to Figs. 1 – 2 . After a 30-min IdU labeling period, medium was changed to medium containing CldU, and cells were incubated an additional... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1255929 | 12707307 | 5 | 200211127f5 | Figure 5.
A similar number of origins localize to fewer DNA fibers at the TDP. (A) Using the fiber preparations collected in Fig. 3 , the percentage of DNA fibers displaying only one versus more than one origin was determined. Results indicate a significant increase in the number of fibers containing two or more bi... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1255929 | 12707307 | 6 | 200211127f6 | Figure 6.
Model for the progressive restriction of initiation potential during G1 phase. In early G1 phase, many sites distributed throughout the genome have an equal potential to be used as early replication origins. At the TDP, late replicating chromosomal domains become excluded from the pool of potential early r... | CC BY-NC-SA | no | 2022-01-13 07:22:09 | J Cell Biol. 2003 Apr 28; 161(2):257-266 | |
PMC1282461 | 15738051 | 1 | 200409187f1 | F igure 1. Sequence alignment of the C-linker regions between CNGA1 and HCN2 and structural model of the C-linker regions of CNGA1. (A) Sequence alignment of the C-linker regions between CNGA1 and HCN2. Green indicates conserved sequence and yellow indicates identical sequence. The square indicates the cysteine mutat... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 2 | 200409187f2 | F igure 2. Cu/P induced potentiation in three of the seven cysteine mutants. Dose–response curves of cysteine mutants and CNGA1 cysless activated by cGMP initially (open circles) and after (filled circles) treatment with Cu/P plus 2 mM cGMP. Smooth curves represent fits with the Hill equation (see materials
and
... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 3 | 200409187f3 | F igure 3. Cu/P effect on the current activated by saturating cAMP. Fraction of the current activated by 20 mM cAMP versus 2 mM cGMP (IcAMP/Imax) initially (open circles) and after Cu/P treatment (filled circles). Points represent the mean, with error bars representing the SEM. Patch numbers range from 4 to 8. Red * ... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 4 | 200409187f4 | F igure 4. DTT reversed the effect of Cu/P treatment. (A) DTT reversed Cu/P potentiation of 417C. cGMP dose–response curves initially (open circles), after a 5-min treatment with Cu/P plus 128 μM cGMP (black circles), and after treatment with 5 mM DTT + 64 μM cGMP for 10 min (red circles). The smooth curves are fits ... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 5 | 200409187f5 | F igure 5. Cu/P produced two populations of channels in 418C. Single channel currents measured at +50 mV were recorded before and after a 10-min treatment with Cu/P plus 2 mM cGMP for 418C (A and B) and CNGA1 cysless channels (C). For 418C, 4 μM cGMP was used to activate the channels, and for CNGA1 cysless , 2 μM cG... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 6 | 200409187f6 | F igure 6. Mechanisms of the dual effects of Cu/P on 418C. (A) Disulfide bonds formed between opposite and adjacent subunits could produce different effects. (B) The number of disulfide bonds could determine whether potentiation or inhibition would be observed. (C and D) Kinetics of the Cu/P effect on 418C with curre... | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1282461 | 15738051 | 7 | 200409187f7 | F igure 7. Cartoon model of closed and open channels. Side (top) and top (bottom) views of the CNGA1 C-linker made from the HCN2 structure (A) and from a model based on our data (B). The A' helices are shown in green and the B' helices are shown in blue. A and B differ only by the conformation of the B'-C' loop. | CC BY-NC-SA | no | 2022-01-13 09:51:40 | J Gen Physiol. 2005 Mar; 125(3):335-344 | |
PMC1283094 | 16103225 | 1 | 200504131f1 | Figure 1.
Targeting of the Sgk3 gene by homologous recombination. (A) Schematic of WT mouse Sgk3 domain structure, gene locus, targeting construct, and mutated Sgk3 allele. Exons 8 and 9 were replaced with PGKneo, and diphtheria toxin A was used for negative selection. Indicated are the antibody binding site, the 5′... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 2 | 200504131f2 | Figure 2.
Sgk3 is required for normal hair coat production. Adult mice (P36 and P411) have a sparse, uneven hair coat (A–D) and irregular hair shafts when seen in profile (E and F). Whiskers are malformed (G and H). Plucked hairs (I and J) lack normal guard, awl, or zigzag hairs. Scanning EM (K and L) shows KO hairs... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 3 | 200504131f3 | Figure 3.
Hair follicle morphogenesis is normal in Sgk3-null mice until P2. At P2, follicles have normal histology by hematoxylin and eosin (A and B), including ORS, IRS, and hair shaft (HS) layers. Follicle number and density is normal (C and D). Differentiation markers AE13 (hair keratins; hair shaft cortex), AE15... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 4 | 200504131f4 | Figure 4.
Anagen maturation is impaired in Sgk3-null hair follicles. Histology is similar at P2 (A and B) but by P6, Sgk3-null follicles are smaller and fail to grow down to the bottom of the subcutis (C and D). At P6, the shortened KO bulb has a smaller, rounded DP relative to the long, thin DP of WT follicles (G a... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 5 | 200504131f5 | Figure 5.
BrdU fate mapping distinguishes between models for reduced bulb cell number and proliferation. (A) Experimental design; mice pulsed with BrdU at P4 were chased for 12 or 20 h. (B) Predicted outcomes for three models. The percentage of Brdu+ cells reflects the percentage of total bulb cells that are BrdU+. ... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 6 | 200504131f6 | Figure 6.
Hair follicles lacking Sgk3 enter catagen prematurely. Histology shows the onset of catagen in WT skin at P15 and in KO skin at P9 (A–J). (EE) Quantification of hair cycle stage based on DP morphology that was visualized by alkaline phosphatase ( Muller-Rover et al., 2001 ). Anagen (alI stages); early cata... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 7 | 200504131f7 | Figure 7.
Growth factor signaling elements are present in the hair follicle. (A) Schematic depicting EGF and IGF-1 pathways and known effects on the anagen to catagen transition. Note the strong evidence that EGF and EGFR promote catagen, which are consistent with the observation that Pten, which is inhibitory to PI... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1283094 | 16103225 | 8 | 200504131f8 | Figure 8.
Growth factor signaling is abnormal in Sgk3-null keratinocytes. (A) Treating WT and KO primary keratinocytes with 10 ng/ml EGF reveals normal kinetics of the activation of ERK 1/2 and Akt. (B) In response to 50 ng/ml IGF-1, Sgk3-null keratinocytes exhibit increased activation of ERK 1/2 and Akt. (C) In pri... | CC BY-NC-SA | no | 2022-01-13 07:26:07 | J Cell Biol. 2005 Aug 15; 170(4):559-570 | |
PMC1289160 | 15767296 | 1 | 200409228f1 | F igure 1. ADP shortens the open time of ΔR/D1370N-CFTR channels. (A) Single-channel current traces in the presence of 1 mM ATP, 1 mM ATP + 1 mM ADP, or 1 mM ATP again. (B) Effects of ADP on the mean open and closed times. Notice that ADP shortens the mean open time and increases the mean closed time ( n = 5). Error... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 2 | 200409228f2 | F igure 2. Macroscopic current relaxation for ΔR/E1371S-CFTR channels in the presence of ATP and ADP. (A) A sample trace of current relaxations for ΔR/E1371S-CFTR channels opened with 1 mM ATP, and subsequently with 1 mM ATP + 2 mM ADP. (B) The current decay upon removal of ATP can be fitted with a single exponential... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 3 | 200409228f3 | F igure 3. Macroscopic current relaxation for ΔR/E1371S-CFTR opened with 10 μM ATP. ΔR/E1371S-CFTR channels were activated with 10 μM ATP until the current reached a steady state. Then the nucleotide was washed out. (A) Sample trace. (B) Ensemble currents were generated by pooling data from 22 experiments. The insets... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 4 | 200409228f4 | F igure 4. Single-channel recording of ΔR/E1371S-CFTR in the presence of 1 μM ATP. A continuous, 54-min single-channel trace in the presence of 1 mM ATP. Note that the channel is open most of the time. The Po is almost 1. | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 5 | 200409228f5 | F igure 5. Single-channel recording of ΔR/E1371S-CFTR in the presence of 10 μM ATP. (A) A continuous 45-min single-channel trace in the presence of 10 μM ATP. Note that the channel remains closed for long periods, and presents opening bursts of different lengths. (B) Expanded traces of selected parts of the trace in ... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 6 | 200409228f6 | F igure 6. Single-channel dwell time analysis of ΔR/E1371S-CFTR. (A) Events from two single-channel recordings (∼50 min each) were pooled together to construct this closed time histogram. The closed time distribution for data obtained at 10 μM ATP can be fitted with a quadruple exponential function. No cutoff was use... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 7 | 200409228f7 | F igure 7. Intraburst kinetic analysis. Locked-open bursts were divided into two categories: short-lived locked-open events (1–50 s in length) and long-lived locked-open events (>50 s). Both types of bursts show similar characteristics. The closed dwell time histograms (A and C) show two components: the flickers (20–... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 8 | 200409228f8 | F igure 8. Macroscopic current relaxation of E1371S-CFTR currents. (A) Sample trace of current relaxations for E1371S-CFTR channels activated with 10 μM ATP + PKA, or with 1 mM ATP + PKA. (B) Normalized ensemble current relaxations upon removal of 1 mM ATP (from 12 patches) or 10 μM ATP (from 9 patches). The 1 mM ATP... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 9 | 200409228f9 | F igure 9. Kinetic analysis of the last E1371S-CFTR channel that remains open after removal of ATP. (A) Sample trace of the current relaxation of E1371S-CFTR channels upon ATP washout. The inset shows the expanded trace of the last channel that remains open. Note the presence of poorly resolved flickers and several l... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 10 | 200409228f10 | F igure 10. The K464A mutation shortens the locked-open time of E1371S-CFTR. (A) Sample trace of K464A/E1371S-CFTR channels in the presence of 1 mM ATP + PKA. Note that the relaxation upon nucleotide washout is very fast. (B) Ensemble macroscopic currents were generated from 18 patches. The macroscopic current has a ... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1289160 | 15767296 | 11 | 200409228f11 | F igure 11. Kinetic analysis of the spontaneous openings in the absence of ATP. (A) A representative ΔR/E1371S-CFTR current trace from an excised inside-out patch exposed to ATP-free solution for several minutes before 1 mM ATP was applied. (B) Similar experiment as described in A, but with ΔR-CFTR channels. The open... | CC BY-NC-SA | no | 2022-01-13 09:52:21 | J Gen Physiol. 2005 Apr; 125(4):377-394 | |
PMC1307503 | 11781335 | 1 | 0110059f1 | Figure 1.
I SOCE during Xenopus oocyte maturation. (A) Voltage protocol used to measure I SOCE development and I–V relationship. The membrane potential was stepped to −140 mV (100 ms), and then ramped from −140 to +60 mV (2 s) from a −40 mV holding potential. The protocol was applied once every 30 s. (B and C) I... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 2 | 0110059f2 | Figure 2.
Time course of MPF, MAPK, and Mos activation during progesterone-induced maturation. (A) Time course of GVBD. GVBD i occurred at 5.5 h, and GVBD 50 ∼7.25 h after progesterone addition. At each time point, five cells were pooled to quantify kinase activity. (B–D) MPF, P-MAPK, and Mos levels during oocyte ... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 3 | 0110059f3 | Figure 3.
Correlation between I
SOCE
and MPF and P-MAPK levels after Δ87cyclin B1 protein injection. Oocytes were either directly injected with Δ87cyclin B1 protein (A and B) or preincubated in the MEK inhibitor PD98059 (50–100 μM) for 0.5–2 h before Δ87cyclin B1 injection. I SOCE levels were recorded at variou... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 4 | 0110059f4 | Figure 4.
Representative individual cell data from Δ87cyclin B1–injected cells. MPF, P-MAPK, and Mos Western data are shown in conjunction with the levels of each kinase in fully mature eggs (EGG). (A) I SOCE was activated in response to store depletion with ionomycin (10 μM) in an oocyte, and MPF, P-MAPK, and Mos ... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 5 | 0110059f5 | Figure 5.
Correlation between I
SOCE
and Mos, P-MAPK, and MPF levels after injection of GST–Mos RNA. GST–Mos is a fusion protein between GST and Xenopus Mos, which allowed the separation between endogenous Mos (39 kD) and recombinant, injected GST–Mos (64 kD) (see Materials and methods). Oocytes were either di... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 6 | 0110059f6 | Figure 6.
Representative individual cell data from Wee1- and Mos-injected cells. MPF, P-MAPK, and Mos Western data are shown in conjunction with the levels of each kinase from a lysate of fully mature eggs (EGG). (A) I SOCE was activated in response to store depletion with ionomycin (10 μM) in an oocyte. MPF, P-MAP... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 7 | 0110059f7 | Figure 7.
Continuous recording of I
SOCE
through the GVBD transition. (A) Prolonged recording of I SOCE from a control untreated oocyte. MPF activity in this cell is also shown. (B) I SOCE was activated in a progesterone-treated oocyte before GVBD and continuously recorded until, and past, the time point at wh... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1307503 | 11781335 | 8 | 0110059f8 | Figure 8.
Pre-activated I
SOCE
does not inactivate in response to MPF activation. Oocytes were incubated in Ca 2+ -free medium (L-15 with Ca 2+ , buffered at 50 μM), containing thapsigargin (1 μM) to deplete intracellular Ca 2+ store and activate I SOCE . Cells were voltage clamped in a Ca 2+ -free solution (70... | CC BY-NC-SA | no | 2022-01-13 07:20:15 | J Cell Biol. 2002 Jan 7; 156(1):75-86 | |
PMC1343528 | 16275756 | 1 | 200505155f1 | Figure 1.
Phosphorylation of the α 1C subunit by CaMKII. (A) Autoradiogram showing phosphorylation of α 1C by CaMKII. Lysates from HEK cells transfected with α 1C and β2b (lanes 2–4) or nontransfected cells (lane 1) were immunoprecipitated with an anti-α 1C antibody (lanes 1, 3, and 4) or control IgG (lane 2) an... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 2 | 200505155f2 | Figure 2.
CaMKII coimmunoprecipitates and colocalizes with α 1C . (A) Biotinylated calmodulin overlay of rat cardiac sarcolemmal membranes after immunoprecipitation with an anti-α 1C antibody. Purified α-CaMKII was run as a control to demonstrate effectiveness of CaM overlay. An anti-α 1C antibody (but not control... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 3 | 200505155f3 | Figure 3.
Activity-dependent interaction of CaMKII with the cytoplasmic determinants of α 1C . Immunoblots using an mAb (CBα2) for CaMKII after a GST pull-down assay with 20 nM of native (top), Ca 2+ /CaM-activated (middle), or Ca 2+ /CaM/autophosphorylated α-CaMKII (bottom). GST fusion proteins contained various cy... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 4 | 200505155f4 | Figure 4.
Localization of the CaMKII binding site on the COOH terminus of α 1C . (A) Diagram of α 1C fusion proteins used in GST pull-down assays with autophosphorylated α-CaMKII, exhibiting robust (+), partial (±), and no (−) binding. (B) Immunoblot with CBα2 after GST pull down of 20 nM of purified autophosphoryl... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 5 | 200505155f5 | Figure 5.
CaMKII interaction with the COOH terminus of α 1C is essential for CDF. (A) I
Ba and scaled I
Ca traces during a train of 40 test pulses of V
h from –90 mV to +20 mV at 3.3 Hz recorded from oocytes expressing α 1C I1654A (I/A) or α 1C I1654A/ 1644 TVGKFY 1649 → EEDAAA (I/A-Mut6). Bars, 500 ... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 6 | 200505155f6 | Figure 6.
The binding site for the COOH terminus of α 1C on CaMKII is localized near the catalytic domain. (A) Biotinylated CaM overlay of GST pull downs, using a fusion protein from the COOH terminus of α 1C (aa 1509–1905) on lysates of HEK 293 cells transiently transfected with the CaMKII isoforms (α, β, δ A , δ... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 7 | 200505155f7 | Figure 7.
CaMKII interaction with the COOH terminus of α 1C is not reversed by dephosphorylation or CaM dissociation, and tethered CaMKII requires autophosphorylation or Ca 2
+
/CaM for activity. (A and B) Immunoblots with CBα2 or a phosphospecific CaMKII mAb after GST pull-down assays, using α 1C aa 1509–1905... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1343528 | 16275756 | 8 | 200505155f8 | Figure 8.
Proposed mechanism of CaMKII binding to α 1C to form a local and dedicated Ca 2
+
spike integrator for CDF. A catalytic core and autoregulatory domain for a prototypical CaMKII inactive subunit is shown on the bottom left (inactive is indicated by green). Ca 2+ /CaM activation and Thr 286 autophospho... | CC BY-NC-SA | no | 2022-01-13 07:26:11 | J Cell Biol. 2005 Nov 7; 171(3):537-547 | |
PMC1350743 | 16314435 | 1 | 20051166f1 | Figure 1. OVA-specific CD4 + CD25 + regulatory T cells regulate allergen-induced airway inflammation in vivo . OVA-sensitized mice received either 5 × 10 5 CD4 + CD25 + cells or an equivalent volume of PBS and were challenged through the airways with OVA. (A) AHR was measured 24 h after the final OVA challenge usin... | CC BY-NC-SA | no | 2022-01-13 09:01:11 | J Exp Med. 2005 Dec 5; 202(11):1539-1547 | |
PMC1350743 | 16314435 | 2 | 20051166f2 | Figure 2. Transfer of CD4 + CD25 + regulatory T cells reduces Th2 cell responses in the lung after allergen challenge. BAL (A) and lung tissue digest cells (B) were isolated as described in Materials and methods. Th2 cell numbers were determined 24 h after the final OVA challenge by antibody staining and flow cytometr... | CC BY-NC-SA | no | 2022-01-13 09:01:11 | J Exp Med. 2005 Dec 5; 202(11):1539-1547 | |
PMC1350743 | 16314435 | 3 | 20051166f3 | Figure 3. Suppression of allergen-induced airway inflammation is IL-10 dependent. Mice were treated with anti–IL-10R antibody or control Ig during the allergen challenge phase of allergic inflammation. AHR (A) and lung eosinophilia (B) were quantified as described in Materials and methods. IL-5 (C), IL-13 (D), and IL-1... | CC BY-NC-SA | no | 2022-01-13 09:01:11 | J Exp Med. 2005 Dec 5; 202(11):1539-1547 | |
PMC1350743 | 16314435 | 4 | 20051166f4 | Figure 4. Transfer of IL-10–deficient CD4 + CD25 + regulatory T cells suppresses allergen-induced airway inflammation. Mice received either wild-type CD4 + CD25 + regulatory T cells, IL-10–deficient CD4 + CD25 + regulatory T cells, or an equivalent volume of PBS as a control. AHR (A) and lung eosinophilia (B) were d... | CC BY-NC-SA | no | 2022-01-13 09:01:11 | J Exp Med. 2005 Dec 5; 202(11):1539-1547 | |
PMC1350743 | 16314435 | 5 | 20051166f5 | Figure 5. IL-10 is produced by CD4 + T cells during allergen-induced airway inflammation and is increased by transfer of CD4 + CD25 + regulatory T cells. Lungs were digested with collagenase and DNase as described in Materials and methods. Digest cells were stimulated by PMA/Ionomycin in the presence of Brefeldin A f... | CC BY-NC-SA | no | 2022-01-13 09:01:11 | J Exp Med. 2005 Dec 5; 202(11):1539-1547 | |
PMC1350947 | 16260490 | 1 | 20051376f1 | Figure 1. Persistent MV infection in the transgene mice. The SSPE tg mouse model was generated by first creating tg mice expressing the MV receptor CD46 (reference 12 ) and then breeding these mice on a Rag1 −/− background (references 19 , 30 ). (A, C, and E–H) MV replication in individual 6–8-wk-old mice given MV ... | CC BY-NC-SA | no | 2022-01-13 09:01:09 | J Exp Med. 2005 Nov 7; 202(9):1185-1190 | |
PMC1350947 | 16260490 | 2 | 20051376f2 | Figure 2. Anatomical location and frequency of 69 A to G hypermutations. The hypermutations were recorded in the MV M gene open reading frame from one representative mouse out of five studied. 12 cDNA clones were isolated, and each position of A to G changes in the MV M is marked with an asterisk. Data showing the A to... | CC BY-NC-SA | no | 2022-01-13 09:01:09 | J Exp Med. 2005 Nov 7; 202(9):1185-1190 | |
PMC1350947 | 16260490 | 3 | 20051376f3 | Figure 3. Data implicating a dual viral hit mechanism for causing persistent MV SSPE-like infection. The first hit is immunosuppressive LCMV Cl 13 given i.v. at a dose of 2 × 10 6 . (A–C) When 10 5 PFU of MV is administered i.c. 10 d later, the neurons of all inoculated mice become persistently infected with MV. LCMV ... | CC BY-NC-SA | no | 2022-01-13 09:01:09 | J Exp Med. 2005 Nov 7; 202(9):1185-1190 | |
PMC1351127 | 15824131 | 1 | 200411118f1 | Figure 1.
ZW10 and Zwint-1 reside in distinct kinetochore subcomplexes in HeLa cells. (A) Localization of ZW10 LAPtag in a HeLa cell line stably expressing the fusion protein (clone LZ5). Cells were treated with nocodazole for 30 min before fixation, and stained for ZW10 LAPtag (anti-GFP), centromeres (ACA), and D... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 2 | 200411118f2 | Figure 2.
Interaction between Zwint-1 and ZW10 controls ZW10 kinetochore localization. (A) Immunoblot of Zwint-1 immunoprecipitates shows weak interaction with ZW10. Cells of clone LINT2.8 were subjected to immunoprecipitation with control antibody (Con) or anti-GFP antibody to precipitate Zwint-1 LAPtag and the pr... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 3 | 200411118f3 | Figure 3.
Characterization of
Xenopus
ZW10 and Rod. (A and B) Schematic alignment of Xenopus and human ZW10 (A) or Xenopus Rod COOH (XL107l09) and human Rod (B). Amino acid positions as well as percentage identity and additional (*) similarity on the protein level are indicated. (C) Coomassie staining of pu... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 4 | 200411118f4 | Figure 4.
The X-ZW10–X-Rod complex is essential for establishment and maintenance of the mitotic checkpoint. (A) Immunoblot of immunodepleted CSF extract. Extracts were depleted with anti–rabbit IgG (ΔIgG), anti–X-ZW10 (ΔX-Z), or anti–X-Rod COOH (ΔX-R). 1 μl of extract or the eluate of 1-μl beads from the immunodep... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 5 | 200411118f5 | Figure 5.
X-ZW10–X-Rod regulate kinetochore localization of X-BubR1, X-Mad1, and X-Mad2. (A–C) Immunolocalization of checkpoint proteins in depleted Xenopus extracts. Unreplicated sperm nuclei in mock (A, ΔIgG) or X-ZW10–X-Rod–depleted (B, ΔX-ZW10; or C, ΔX-Rod) extracts were immunostained with antibodies to the i... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 6 | 200411118f6 | Figure 6.
Human ZW10 is essential for mitotic checkpoint signaling. (A) Immunoblot analysis of ZW10 knockdown. HeLa cells were transfected with control or ZW10 siRNA duplexes. 5 d after transfection, total lysates were analyzed for ZW10 and tubulin protein. Percentage knockdown was determined by serial dilution immu... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351127 | 15824131 | 7 | 200411118f7 | Figure 7.
Mad1 and Mad2 are unable to bind kinetochores in absence of ZW10. (A–F) Immunolocalization of various proteins in ZW10-depleted cells. HeLa cells were transfected as in Fig. 6 A and treated with nocodazole 30 min before fixation. Cells were stained with ACA (A, B, and C), ZW10 (A, B, D, and F), and dynei... | CC BY-NC-SA | no | 2022-01-13 07:23:19 | J Cell Biol. 2005 Apr 11; 169(1):49-60 | |
PMC1351290 | 15753208 | 1 | 20041470f1 | Figure 1. Serum reconstitution of J H mice. Lesion size of J H mice (closed triangles) and BALB/c mice (closed circles) was compared with J H mice (open triangles) and BALB/c mice (open circles) given 200 μl of antisera to L. major on days 1, 7, and 14. Parasite burdens (inset) in BALB/c and J H mice that were in... | CC BY-NC-SA | no | 2022-01-13 09:00:57 | J Exp Med. 2005 Mar 7; 201(5):747-754 | |
PMC1351290 | 15753208 | 2 | 20041470f2 | Figure 2. Serum reconstitution of J H mice 3 wk after infection. Lesion size of J H mice (closed circles) were compared with those of J H mice given 200 μl αLm (α– L. major ) antiserum on day 21 after infection (open circles). Parasite burdens (inset) were determined at 42 d after infection by limiting dilution assa... | CC BY-NC-SA | no | 2022-01-13 09:00:57 | J Exp Med. 2005 Mar 7; 201(5):747-754 | |
PMC1351290 | 15753208 | 3 | 20041470f3 | Figure 3. Cytokine production in mice administered anti– L. major antiserum. (A) Cytokine production by lymph node T cells from infected J H mice (white bars) was compared with J H mice administered 200 μl αLm (α– L. major ) antiserum on days 1, 7, and 14 after infection (black bars). Lymph nodes were removed on day... | CC BY-NC-SA | no | 2022-01-13 09:00:57 | J Exp Med. 2005 Mar 7; 201(5):747-754 | |
PMC1351290 | 15753208 | 4 | 20041470f4 | Figure 4. IgG reconstitution of J H mice and the effect of α–IL-10R mAb. Three parallel groups of J H mice were infected with 2 × 10 5
L. major amastigotes. One group (open circles) was administered 600 μg of purified αLm-IgG i.p. on days 1, 8, and 15. Another group (gray triangles) was given the same dose of αLm-... | CC BY-NC-SA | no | 2022-01-13 09:00:57 | J Exp Med. 2005 Mar 7; 201(5):747-754 | |
PMC1351290 | 15753208 | 5 | 20041470f5 | Figure 5. The immunization of C57BL/6 mice with OVA. Lesion development in OVA-immunized mice (open circles) was compared with control mice given IFA alone (closed circles). Immunized mice were given 25 μg OVA in 500 μL of IFA and boosted 2 wk later. Both groups of mice were infected with L. major resuspended in PBS ... | CC BY-NC-SA | no | 2022-01-13 09:00:57 | J Exp Med. 2005 Mar 7; 201(5):747-754 |
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