Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1210/me.2014-1024 http://scihub22266oqcxt.onion/10.1210/me.2014-1024 C4154244!4154244 !25073103     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25073103 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25073103 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Endocrinol 2014 ; 28 (9 ): 1435-47 Nephropedia Template TP {{tp|p=25073103 |t=2014. Activated FoxM1 attenuates streptozotocin-mediated ?-cell death |pdf=|usr=}}{{25073103 }} gab.com Text Activated FoxM1 attenuates streptozotocin-mediated -cell death JO: Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=25073103 #FOAvip The forkhead box transcription factor FoxM1, a positive regulator of the cell cycle, is required for ?-cell mass expansion postnatally, during pregnancy, and after partial pancreatectomy. Up-regulation of full-length FoxM1, however, is unable to stimulate increases in ?-cell mass in unstressed mice or after partial pancreatectomy, probably due to the lack of posttranslational activation. We hypothesized that expression of an activated form of FoxM1 could aid in recovery after ?-cell injury. We therefore derived transgenic mice that inducibly express an activated version of FoxM1 in ?-cells (RIP-rtTA;TetO-hemagglutinin (HA)-Foxm1(?)(NRD) mice). This N-terminally truncated form of FoxM1 bypasses 2 posttranslational controls: exposure of the forkhead DNA binding domain and targeted proteasomal degradation. Transgenic mice were subjected to streptozotocin (STZ)-induced ?-cell ablation to test whether activated FoxM1 can promote ?-cell regeneration. Mice expressing HA-FoxM1(?NRD) displayed decreased ad libitum-fed blood glucose and increased ?-cell mass. ?-Cell proliferation was actually decreased in RIP-rtTA:TetO-HA-Foxm1(NRD) mice compared with that in RIP-rtTA mice 7 days after STZ treatment. Unexpectedly, ?-cell death was decreased 2 days after STZ treatment. RNA sequencing analysis indicated that activated FoxM1 alters the expression of extracellular matrix and immune cell gene profiles, which may protect against STZ-mediated death. These studies highlight a previously underappreciated role for FoxM1 in promoting ?-cell survival. Twit Text FOAVip Activated FoxM1 attenuates streptozotocin-mediated -cell death ????Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=25073103 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25073103 #FOAvip English Wikipedia <ref>{{Cite pmid|25073103 }}</ref> Activated FoxM1 attenuates streptozotocin-mediated ?-cell death #MMPMID25073103 Golson ML ; Maulis MF ; Dunn JC ; Poffenberger G ; Schug J ; Kaestner KH ; Gannon MA Mol Endocrinol 2014[Sep]; 28 (9 ): 1435-47 PMID25073103 show ga The forkhead box transcription factor FoxM1, a positive regulator of the cell cycle, is required for ?-cell mass expansion postnatally, during pregnancy, and after partial pancreatectomy. Up-regulation of full-length FoxM1, however, is unable to stimulate increases in ?-cell mass in unstressed mice or after partial pancreatectomy, probably due to the lack of posttranslational activation. We hypothesized that expression of an activated form of FoxM1 could aid in recovery after ?-cell injury. We therefore derived transgenic mice that inducibly express an activated version of FoxM1 in ?-cells (RIP-rtTA;TetO-hemagglutinin (HA)-Foxm1(?)(NRD) mice). This N-terminally truncated form of FoxM1 bypasses 2 posttranslational controls: exposure of the forkhead DNA binding domain and targeted proteasomal degradation. Transgenic mice were subjected to streptozotocin (STZ)-induced ?-cell ablation to test whether activated FoxM1 can promote ?-cell regeneration. Mice expressing HA-FoxM1(?NRD) displayed decreased ad libitum-fed blood glucose and increased ?-cell mass. ?-Cell proliferation was actually decreased in RIP-rtTA:TetO-HA-Foxm1(NRD) mice compared with that in RIP-rtTA mice 7 days after STZ treatment. Unexpectedly, ?-cell death was decreased 2 days after STZ treatment. RNA sequencing analysis indicated that activated FoxM1 alters the expression of extracellular matrix and immune cell gene profiles, which may protect against STZ-mediated death. These studies highlight a previously underappreciated role for FoxM1 in promoting ?-cell survival. |Animals [MESH] |Cell Cycle [MESH] |Cell Death [MESH] |Cell Proliferation [MESH] |Cell Survival [MESH] |Diabetes Mellitus/metabolism [MESH] |Female [MESH] |Forkhead Box Protein M1 [MESH] |Forkhead Transcription Factors/*metabolism [MESH] |Immune System [MESH] |Insulin-Secreting Cells/cytology/*metabolism/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Regeneration [MESH] |Sequence Analysis, RNA [MESH]Activated FoxM1 attenuates streptozotocin-mediated ?-cell death (epmc).pdf DeepDyve Pubget Overpricing