ArticleCellular signalling2010
STAT1 activation regulates proliferation and differentiation of renal progenitors.
Article in Cellular signalling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Evaluation of molecular profiles in calcineurin inhibitor toxicity post-kidney transplant: input to chronic allograft dysfunction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2014Trial
- G protein‑coupled receptor kinase 4 governs early kidney development via STAT3 and Nhe3a.International journal of molecular medicine · 2026Article
- A STAT1-GBP1 axis modulates epithelial proliferation in postpartum breast tissue by repressing CDKI expression.Breast cancer research : BCR · 2025Article
- Elevated Type I Interferon Signaling Defines the Proliferative Advantage of ARF and p53 Mutant Tumor Cells.Molecular and cellular biology · 2025Article
- Measurement of adhesion and traction of cells at high yield reveals an energetic ratchet operating during nephron condensation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Measurement of adhesion and traction of cells at high yield (MATCHY) reveals an energetic ratchet driving nephron condensation.bioRxiv : the preprint server for biology · 2024Article
- Nephron progenitors rhythmically alternate between renewal and differentiation phases that synchronize with kidney branching morphogenesis.bioRxiv : the preprint server for biology · 2024Article
- Proteomimetics of Natural Regulators of JAK-STAT Pathway: Novel Therapeutic Perspectives.Frontiers in molecular biosciences · 2021Review
- Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer.Cancer biology & therapy · 2020Article
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- FIH-1 engages novel binding partners to positively influence epithelial proliferation via p63.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A brief overview of antitumoral actions of bruceine D.Exploration of targeted anti-tumor therapy · 2020Review
- MSC Transplantation Improves Lacrimal Gland Regeneration after Surgically Induced Dry Eye Disease in Mice.Scientific reports · 2019Article
- PIAS1 is not suitable as a urothelial carcinoma biomarker protein and pharmacological target.PloS one · 2019Article
- Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression.PloS one · 2018Article
- Preferential Propagation of Competent SIX2+ Nephronic Progenitors by LIF/ROCKi Treatment of the Metanephric Mesenchyme.Stem cell reports · 2015Article
- STING Negatively Regulates Double-Stranded DNA-Activated JAK1-STAT1 Signaling via SHP-1/2 in B Cells.Molecules and cells · 2015Article
- Non-canonical Wnt5a/Ror2 signaling regulates kidney morphogenesis by controlling intermediate mesoderm extension.Human molecular genetics · 2014Article
- Article
- Protein/peptide transduction in metanephric explant culture.Methods in molecular biology (Clifton, N.J.) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We have shown previously that activation of STAT1 contributes to the pathogenesis of Wilms tumor. This neoplasm caricatures metanephric development and is believed to originate from embryonic renal mesenchymal progenitors that lose their ability to undergo mesenchymal-epithelial transition (MET). Therefore, we hypothesized that STAT1 is also activated and functional during metanephric development. Here we have demonstrated that both STAT1 and STAT3 are activated during normal development of the embryonic kidney. Furthermore, activation of STAT1 stimulated the proliferation of metanephric mesenchymal cells, but it prevented MET and tubulogenesis induced by leukemia inhibitory factor, which preferentially activates STAT3. Consistent with its negative regulation of metanephric mesenchymal differentiation, inhibition of STAT1 activation with protein kinase CK2 inhibitor TBB or RNAi-mediated knockdown of STAT1 promoted differentiation of metanephric progenitors and abolished the effect of cytokine-induced STAT1 activation in these cells. Additionally, a cell-permeable peptide that inhibits STAT1-mediated transactivation by targeting the STAT1 N-domain also blocked cytokine-induced STAT1-dependent proliferation in metanephric progenitors and promoted LIF-induced MET and tubulogenesis. Finally, the STAT1 peptide inhibitor caused the down regulation of survival/anti-apoptotic factors, Mcl-1 and Hsp-27, and induced apoptosis in renal tumor cells with constitutively active STAT1, indicating that STAT1 is required for these cells to survive. These findings show that both metanephric progenitors and renal tumor cells utilize a STAT1-dependent mechanism for growth or survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.