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10.1101/gad.237149.113 http://scihub22266oqcxt.onion/10.1101/gad.237149.113 24732380!4018495!24732380     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Genes+Dev 2014 ; 28 (9): 971-82 Nephropedia Template TP {{tp|p=24732380|t=2014. Lin28 sustains early renal progenitors and induces Wilms tumor |pdf=|usr=}}{{24732380}} gab.com Text Lin28 sustains early renal progenitors and induces Wilms tumor JO: Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=24732380 #FOAvip Wilms Tumor, the most common pediatric kidney cancer, evolves from the failure of terminal differentiation of the embryonic kidney. Here we show that overexpression of the heterochronic regulator Lin28 during kidney development in mice markedly expands nephrogenic progenitors by blocking their final wave of differentiation, ultimately resulting in a pathology highly reminiscent of Wilms tumor. Using lineage-specific promoters to target Lin28 to specific cell types, we observed Wilms tumor only when Lin28 is aberrantly expressed in multiple derivatives of the intermediate mesoderm, implicating the cell of origin as a multipotential renal progenitor. We show that withdrawal of Lin28 expression reverts tumorigenesis and markedly expands the numbers of glomerulus-like structures and that tumor formation is suppressed by enforced expression of Let-7 microRNA. Finally, we demonstrate overexpression of the LIN28B paralog in a significant percentage of human Wilms tumor. Our data thus implicate the Lin28/Let-7 pathway in kidney development and tumorigenesis. Twit Text FOAVip Lin28 sustains early renal progenitors and induces Wilms tumor ????Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=24732380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24732380 #FOAvip English Wikipedia <ref>{{Cite pmid|24732380}}</ref> Lin28 sustains early renal progenitors and induces Wilms tumor #MMPMID24732380 Urbach A; Yermalovich A; Zhang J; Spina CS; Zhu H; Perez-Atayde AR; Shukrun R; Charlton J; Sebire N; Mifsud W; Dekel B; Pritchard-Jones K; Daley GQ Genes Dev 2014[May]; 28 (9): 971-82 PMID24732380show ga Wilms Tumor, the most common pediatric kidney cancer, evolves from the failure of terminal differentiation of the embryonic kidney. Here we show that overexpression of the heterochronic regulator Lin28 during kidney development in mice markedly expands nephrogenic progenitors by blocking their final wave of differentiation, ultimately resulting in a pathology highly reminiscent of Wilms tumor. Using lineage-specific promoters to target Lin28 to specific cell types, we observed Wilms tumor only when Lin28 is aberrantly expressed in multiple derivatives of the intermediate mesoderm, implicating the cell of origin as a multipotential renal progenitor. We show that withdrawal of Lin28 expression reverts tumorigenesis and markedly expands the numbers of glomerulus-like structures and that tumor formation is suppressed by enforced expression of Let-7 microRNA. Finally, we demonstrate overexpression of the LIN28B paralog in a significant percentage of human Wilms tumor. Our data thus implicate the Lin28/Let-7 pathway in kidney development and tumorigenesis. |*Cell Differentiation[MESH] |Animals[MESH] |Gene Expression[MESH] |Gene Expression Regulation, Developmental[MESH] |Humans[MESH] |Kidney Neoplasms/*genetics/*physiopathology[MESH] |Kidney/embryology[MESH] |Mice[MESH] |MicroRNAs/genetics/metabolism[MESH] |RNA-Binding Proteins/*genetics/metabolism[MESH] |Stem Cells/*cytology[MESH]Lin28 sustains early renal progenitors and induces Wilms tumor (epmc).pdf DeepDyve Pubget Overpricing