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"...e JCI" /> <input alt="Search black" type="image" src="/assets/search-black-867f68b5b717d00fb9c106b8c637cfd33ea8ee8b2ff37a9eaf8cc675abe2fc86.png" value="" /> </for..."

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"...columns'> <a href='https://www.jci.org/articles/view/90647/figure/1' ref='group' title='In vivo effects of G-CSF in irradiated mice. (A) Immunohistochemical assessment of BrdU+ neural progenitors in the lateral SVZ and DG of the brain from mice treated with PBS or G-CSF or whole-body–irradiated mice (4.5 Gy) treated with PBS or G-CSF. G-CSF was injected on days 1, 3, and 5 after irradiation. At day 5, BrdU was injected, and mice were sacrificed 2 hours after injection. Original magnification: ×20. (B) Quantification of BrdU+ cells from the SVZ, DG, and CC. Asterisks indicate a significant change relative to control. *P &lt; 0.05; ***P &lt; 0.001; ****P &lt; 0.0001, 2-way ANOVA. n = 6–8 independent biological replicates. Data are presented as mean ± SEM of biological replicates. (C) Quantification of Nestin+ cells in the brain (SVZ and DG) of nonirradiated mice treated with G-CSF. Asterisks indicate a significant change relative to control. *P &lt; 0.05; ***P &lt; 0.001, Student’s t test. n = 3 independent biological replicates. Data are presented as mean ± SEM of biological replicates.'> <img ..." Line: 434 Column: 1 - 1088
"...columns'> <a href='https://www.jci.org/articles/view/90793/figure/1' ref='group' title='Genome-scale CRISPR-Cas9 screen reveals neuroblastoma dependency on the PRC2 complex components EZH2, EED, and SUZ12. (A) Projection of the 341 cancer cell lines on the top 3 independent components (IC1, IC2, IC3) that are enriched for depletion in neuroblastoma (red) versus other cell lines (gray). (B) Rank of IC3 component genes by the gene Z score in the component with rank in parentheses. (C) Neuroblastoma is the cancer type with the most depletion in the CRISPR-Cas9 screen for the EED/EZH2 complex based on single-sample enrichment analysis. (D and E) Immunoblot (D) and cell viability assay (E) after CRISPR-Cas9 knockout of EZH2 with 4 EZH2 sgRNAs in SK-N-BE(2). Results are representative of 3 independent experiments; mean ± SD of 8 technical replicates is shown. (F and G) Immunoblot (F) and cell viability assay (G) after shRNA-mediated suppression of EZH2 in SK-N-BE(2), Kelly, and LAN-1. Results are representative of 3 independent experiments; mean ± SD of 8 technical replicates is shown.'> <img ..." Line: 506 Column: 1 - 1698
"...columns'> <a href='https://www.jci.org/articles/view/92513/figure/1' ref='group' title='GDF6 is recurrently amplified and specifically expressed in melanomas. (A) Circos plot displaying gene copy number gains and losses of zebrafish melanomas across 25 chromosomes. JISTIC G-scores are displayed as pale red shading (amplifications [minimum = 0; maximum = 1,550]) and blue shading (deletions [minimum = 0; maximum = 2,150]). –log10-transformed JISTIC Q-values with a cutoff of 0.6 (corresponding to an untransformed Q-value of 0.25) are shown as bold red lines (amplifications [minimum = 0; maximum = 11]) and bold blue (deletions [minimum = 0; maximum = 11]). Dotted circles represent the –log10-transformed Q-value of 0 (center) and 11 (outer: amplification; inner: deletion). (B) Venn diagram of orthologous genes significantly amplified in human and zebrafish melanomas from a total of 10,380 human-zebrafish gene pairs (hypergeometric test, P value: 2.0 × 10–15). (C) Genes significantly upregulated in zebrafish melanomas as compared with melanocytes (microarray data set) are plotted in order of their fold change. Only genes with a fold change of greater than 2 and an adjusted P value of less than 0.05 are plotted. Recurrently amplified genes with amplified human orthologs are indicated in red. gdf6b (large red dot) and gdf6a (large black dot) are indicated. Dashed horizontal line represents a fold change of 2. (D) Immunostaining of Tg(mitfa:BRAFV600E);p53(lf) zebrafish scales bearing melanoma cells or normal melanocytes. DAPI (blue), Gdf6b (green), Mitfa (red), and a merged image of all channels are shown. Mitfa antibody specificity is shown in Supplemental Figure 2B. Scale bars: 10 μm.'> <img ..." Line: 578 Column: 1 - 730
"...columns'> <a href='https://www.jci.org/articles/view/93566/figure/1' ref='group' title='RB loss is frequent in CRPC and can be detected in circulating tumor DNA. (A) Mutual exclusivity plot indicating presence or absence of multiple alterations with each sample in the SU2C cohort (left) and frequency of indicated alterations in SU2C CRPC cohort (n = 144, right). CNA, copy number alteration. (B) Prevalence of specific RB alterations. (C) Schematic of ctDNA collection and sequencing of CRPC samples by the Karolinska Institute (top) and copy number alterations in RB pathway genes identified within the Karolinska ctDNA cohort through sequencing of a 1.3-Mb panel (bottom left) and prevalence of specific RB alterations (bottom right).'> <img ..." Line: 650 Column: 1 - 903
"...columns'> <a href='https://www.jci.org/articles/view/93597/figure/1' ref='group' title='Mesenchymal loss of Lkb1 is sufficient to drive fully penetrant PJS polyposis in mice. (A) Representative macroscopic images of wild-type, Lkb1+/–, Lkb1TwKO/+, and Lkb1FspKO/+ mouse stomachs at 11 months of age. Scale bars: 5 mm. (B) Survival curve of Lkb1+/– (n = 15), Lkb1TwKO/+ (TwKO/+, n = 7), and Lkb1FspKO/+ mice (FspKO/+, n = 27). Lkb1FspKO/+ mice were followed until 17 months, with no mortality observed. (C and D) Comparison of polyp number (nr) (C) and diameter (D) in Lkb1+/– (n = 15), Lkb1TwKO/+ (TwKO/+, n = 6), and Lkb1FspKO/+ mice (FspKO/+, n = 8) at 11 months of age. Lines depict mean and standard deviation. (E) Cre activity representing Lkb1 heterozygous cells as depicted by GFP signal in Lkb1TwKO/+;R26R-mTmG mouse antral polyp. Representative image is shown. Scale bars: 500 μm and 100 μm (zoom-ins).'> <img ..." Line: 722 Column: 1 - 848
"...columns'> <a href='https://www.jci.org/articles/view/94509/figure/1' ref='group' title='hSTAT5BN642H is an activating mutation. (A) Schematic of STAT5B mutations identified in leukemia and lymphoma patients. Each dot represents 1 patient. (B) WB analysis of pY-STAT5, total STAT5 protein, and HSC70 in 293T cells that were transiently transfected with different hSTAT5B (hS5B) variants using a pMSCV-IRES-GFP vector, with or without growth hormone (GH) stimulation. (C) WB analysis of pY-STAT5, STAT5, FLAG, and HSC70 in hSTAT5B- or hSTAT5BN642H-expressing (N642H) Ba/F3 cells with or without IL-3 stimulation. (B and C) Nontransfected and pMSCV-transfected cells are shown as controls. Data presented in B and C are representative of 3 independent experiments. Samples were run on parallel gels for B and C, and a loading control is provided for each gel.'> <img ..." Line: 794 Column: 1 - 1378
"...columns'> <a href='https://www.jci.org/articles/view/95837/figure/1' ref='group' title='Syk plays a dominant role in γδTCR signaling and γδT cell development. (A and B) Flow cytometric analysis of CD3ε and TCRδ expression in thymocytes from the indicated mice at E15.5 (WT, n = 16; Zap70–/–, n = 10; Sykb–/–, n = 8; and Zap70–/– Sykb–/–, n = 2) and on day 0 (WT, n = 19; Zap70–/–, n = 4; Sykb–/–, n = 7; and Zap70–/– Sykb–/–, n = 8). The total number of thymocytes is indicated above each flow cytometric plot (A). Graphs indicate the total number of γδT cells per mouse (B). (C and D) TCR-induced ERK phosphorylation in thymic γδT cells from the indicated mice on day 0 (Zap70–/–, n = 3; Sykb–/–, n = 4; and Zap70–/– Sykb–/–, n = 3). Histograms indicate p-ERK levels after a 2-minute stimulation (C). MFI relative to the nonstimulated control (D). (E) Histograms show CD5 expression in thymic γδT cells from the indicated mice at E15.5 (WT, n = 13; Zap70–/–, n = 10; Sykb–/–, n = 9; and Zap70–/– Sykb–/–, n = 2) and on day 0 (WT, n = 17; Zap70–/–, n = 3; Sykb–/–, n = 7; and Zap70–/– Sykb–/–, n = 5). Graphs indicate the MFI relative to WT mice. All data represent the mean ± SEM. *P &lt; 0.05 and **P &lt; 0.01, by 1-way ANOVA (B and E) and 2-way ANOVA (D). Data represent the combined results of 3 independent experiments (A, B, and E) or a single experiment (C and D). Max, maximum.'> <img ..." Line: 866 Column: 1 - 1849
"...columns'> <a href='https://www.jci.org/articles/view/96499/figure/1' ref='group' title='Behavioral, electrophysiological, and pathological improvement after ASO treatment in C22 model. Five-week-old C22 mice were treated with weekly subcutaneous injections of PB, control ASO (CTRL; 50 mg/kg), or ASO1 at 25, 50, or 100 mg/kg per week for 9 weeks. n = 8 per group. WT littermates treated with PBS were included as controls. n = 8. CTRL, control. (A and B) Human PMP22 and mouse Pmp22 mRNA levels in sciatic nerves of treated mice. One-way ANOVA with Dunnett’s post test. *P &lt; 0.05; **P &lt; 0.01; ***P &lt; 0.001. (C) The hind limb grip strength (g) and (D) time remaining on rotarod (s) were measured before treatment began (pretreatment) and at 3, 6, and 9 weeks following treatment. Two-way ANOVA with Tukey’s post test was used to compare pretreated C22 vs. WT (#P &lt; 0.05) or pretreated and posttreated disease groups. *P &lt; 0.05; **P &lt; 0.01; ***P &lt; 0.001. (E) MNCV was measured at pretreatment and at 9 weeks following treatment. Two-way ANOVA with Tukey’s post test was used to compare pretreated C22 versus WT (#P &lt; 0.05) or pretreated and posttreated disease groups. ***P &lt; 0.001. (F) CMAP was measured at 9 weeks after treatment. ASO1-treated groups were compared with PBS group using 1-way ANOVA with Dunnett’s post test. *P &lt; 0.05. (G) Representative electrophysiological trace and (H) representative histological images of cross-sectioned sciatic nerves of a WT treated with PBS, a C22 treated with PBS, or a C22 treated with 100 mg/kg of ASO1 for 9 weeks. Scale bar: 5 μm. (I) Quantification of percentage of myelinated, percentage of unmyelinated, and percentage of onion bulb axons. One-way ANOVA with Dunnett’s post test was used to compare between C22 treated with PBS or ASO1 and WT treated with PBS. ***P &lt; 0.001'> <img ..." Line: 935 Column: 1 - 860
"...columns'> <a href='https://www.jci.org/articles/view/96551/figure/1' ref='group' title='SPOP mutation does not result in ERG protein expression by immunohistochemistry in normal or neoplastic murine prostate. (A) Histologically normal prostate from mice conditionally expressing SPOP-F133V in the prostate (Rosa26SPOP-F133V Pten+/+ Pb-Cre). A and B scale bars: 50 μm. (B) SPOP-mutation-driven murine HG-PIN (Rosa26SPOP-F133V PtenL/+ Pb-Cre). (C) SPOP-mutation-driven murine prostate adenocarcinoma. (Rosa26SPOP-F133V PtenL/L Pb-Cre). Insets show ERG staining in endothelial cells (arrow) adjacent to SPOP-mutant-expressing prostate cells. SPOP-F133V transgenic expression confirmed by GFP expression. A minimum of 3 mice were utilized for each condition. Representative sections are shown. Scale bars: 50 μm in right images of C, 500 μm in left and center images of C.'> <img ..." Line: 1001 Column: 1 - 476
"...columns'> <a href='https://www.jci.org/articles/view/98617/figure/1' ref='group' title='ASO therapy for patients with CMT1A causes demyelination that over time leads to secondary axonal degeneration and ff accumulation in the muscle. ASO binding to PMP22 mRNA may alleviate demyelination, but may not reduce axonal degeneration and ff accumulation in muscle that have already occurred, supporting the use of ASO as early as feasible to minimize these secondary complications of CMT1A.'> <img ..." Line: 1067 Column: 1 - 1403
"...columns'> <a href='https://www.jci.org/articles/view/98619/figure/1' ref='group' title='STAT-mediated oncogenesis. Under physiologic conditions, STAT signaling is stimulus dependent and tightly regulated by endogenous inhibitors, including SOCS proteins, protein inhibitor of activated STAT (PIAS) proteins, and protein tyrosine phosphatases (PTPs). Cytokine or growth factor stimulation triggers receptor oligomerization and sequential tyrosine phosphorylation of receptor-associated JAKs, intracellular receptor domains, and newly recruited STAT proteins. Phosphorylated STAT dimers then translocate to the nucleus, where they bind DNA and control the expression of genes regulating proliferation, survival, and differentiation. Following dephosphorylation, STATs are shuttled back out of the nucleus, completing the activation-inactivation cycle. Cancer-associated events can lead to constitutive STAT activity and STAT-dependent oncogenesis. This can occur through increased STAT activation due to elevated cytokine levels, loss of endogenous inhibitors, or hyperactivation of upstream signaling machinery, or via decreased STAT inactivation, such as that occurring through loss of endogenous inhibitors and dephosphorylation-resistant STAT mutants. The STAT5 mutant STAT5BN642H analyzed by Pham et al. (18) appears to drive the malignant transformation of hematopoietic cells through this latter mechanism.'> <img ..."

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"...icates.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/90000/90647/small/JCI90647.f1.gif'> </a> ..." Line: 435 Column: 1 - 88
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"...right).'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/93000/93566/small/JCI93566.f1.gif'> </a> ..." Line: 651 Column: 1 - 88
"...m-ins).'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/93000/93597/small/JCI93597.f1.gif'> </a> ..." Line: 723 Column: 1 - 88
"...ch gel.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/94000/94509/small/JCI94509.f1.gif'> </a> ..." Line: 795 Column: 1 - 88
"...aximum.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/95000/95837/small/JCI95837.f1.gif'> </a> ..." Line: 867 Column: 1 - 88
"...; 0.001'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/96000/96499/small/JCI96499.f1.gif'> </a> ..." Line: 936 Column: 1 - 88
"...s of C.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/96000/96551/small/JCI96551.f1.gif'> </a> ..." Line: 1002 Column: 1 - 88
"... CMT1A.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/98000/98617/small/JCI98617.f1.gif'> </a> ..." Line: 1068 Column: 1 - 88
"...hanism.'> <img src='//dm5migu4zj3pb.cloudfront.net/manuscripts/98000/98619/small/JCI98619.f1.gif'> </a> ..."

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