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10.1038/cdd.2013.177 http://scihub22266oqcxt.onion/10.1038/cdd.2013.177 C3950320!3950320 !24336047     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\24336047 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Death+Differ 2014 ; 21 (4 ): 568-81 Nephropedia Template TP {{tp|p=24336047 |t=2014. Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation |pdf=|usr=}}{{24336047 }} gab.com Text Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip Calcium deficiency causes abnormal colonic growth and increases colon cancer risk with poorly understood mechanisms. Here we elucidate a novel signaling mechanism underlying the Ca(2+) deficiency-induced epithelial proliferation using a unique animal model. The zebrafish larval yolk sac skin contains a group of Ca(2+)-transporting epithelial cells known as ionocytes. Their number and density increases dramatically when acclimated to low [Ca(2+)] environments. BrdU pulse-labeling experiments suggest that low [Ca(2+)] stimulates pre-existing ionocytes to re-enter the cell cycle. Low [Ca(2+)] treatment results in a robust and sustained activation of IGF1R-PI3K-Akt signaling in these cells exclusively. These ionocytes specifically express Igfbp5a, a high-affinity and specific binding protein for insulin-like growth factors (IGFs) and the Ca(2+)-selective channel Trpv5/6. Inhibition or knockdown of Igfbp5a, IGF1 receptor, PI3K, and Akt attenuates low [Ca(2+)]-induced ionocyte proliferation. The role of Trpv5/6 was investigated using a genetic mutant, targeted knockdown, and pharmacological inhibition. Loss-of-Trpv5/6 function or expression results in elevated pAkt levels and increased ionocyte proliferation under normal [Ca(2+)]. These increases are eliminated in the presence of an IGF1R inhibitor, suggesting that Trpv5/6 represses IGF1R-PI3K-Akt signaling under normal [Ca(2+)]. Intriguingly, blockade of Trpv5/6 activity inhibits the low [Ca(2+)]-induced activation of Akt. Mechanistic analyses reveal that the low [Ca(2+)]-induced IGF signaling is mediated through Trpv5/6-associated membrane depolarization. Low extracellular [Ca(2+)] results in a similar amplification of IGF-induced PI3K-PDK1-Akt signaling in human colon cancer cells in a TRPV6-dependent manner. These results uncover a novel and evolutionarily conserved signaling mechanism that contributes to the abnormal epithelial proliferation associated with Ca(2+) deficiency. Twit Text FOAVip Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip English Wikipedia <ref>{{Cite pmid|24336047 }}</ref> Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation #MMPMID24336047 Dai W ; Bai Y ; Hebda L ; Zhong X ; Liu J ; Kao J ; Duan C Cell Death Differ 2014[Apr]; 21 (4 ): 568-81 PMID24336047 show ga Calcium deficiency causes abnormal colonic growth and increases colon cancer risk with poorly understood mechanisms. Here we elucidate a novel signaling mechanism underlying the Ca(2+) deficiency-induced epithelial proliferation using a unique animal model. The zebrafish larval yolk sac skin contains a group of Ca(2+)-transporting epithelial cells known as ionocytes. Their number and density increases dramatically when acclimated to low [Ca(2+)] environments. BrdU pulse-labeling experiments suggest that low [Ca(2+)] stimulates pre-existing ionocytes to re-enter the cell cycle. Low [Ca(2+)] treatment results in a robust and sustained activation of IGF1R-PI3K-Akt signaling in these cells exclusively. These ionocytes specifically express Igfbp5a, a high-affinity and specific binding protein for insulin-like growth factors (IGFs) and the Ca(2+)-selective channel Trpv5/6. Inhibition or knockdown of Igfbp5a, IGF1 receptor, PI3K, and Akt attenuates low [Ca(2+)]-induced ionocyte proliferation. The role of Trpv5/6 was investigated using a genetic mutant, targeted knockdown, and pharmacological inhibition. Loss-of-Trpv5/6 function or expression results in elevated pAkt levels and increased ionocyte proliferation under normal [Ca(2+)]. These increases are eliminated in the presence of an IGF1R inhibitor, suggesting that Trpv5/6 represses IGF1R-PI3K-Akt signaling under normal [Ca(2+)]. Intriguingly, blockade of Trpv5/6 activity inhibits the low [Ca(2+)]-induced activation of Akt. Mechanistic analyses reveal that the low [Ca(2+)]-induced IGF signaling is mediated through Trpv5/6-associated membrane depolarization. Low extracellular [Ca(2+)] results in a similar amplification of IGF-induced PI3K-PDK1-Akt signaling in human colon cancer cells in a TRPV6-dependent manner. These results uncover a novel and evolutionarily conserved signaling mechanism that contributes to the abnormal epithelial proliferation associated with Ca(2+) deficiency. |Animals [MESH] |Caco-2 Cells [MESH] |Calcium/*pharmacology [MESH] |Cell Proliferation/drug effects [MESH] |Epithelial Cells/cytology/drug effects/*metabolism [MESH] |Humans [MESH] |Insulin-Like Growth Factor I/pharmacology [MESH] |Insulin-Like Growth Factor II/pharmacology [MESH] |Larva/cytology [MESH] |Oligonucleotides, Antisense/metabolism [MESH] |Phosphatidylinositol 3-Kinase/genetics/metabolism [MESH] |Phosphoinositide-3 Kinase Inhibitors [MESH] |Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/metabolism [MESH] |Receptor, IGF Type 1/antagonists & inhibitors/genetics/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Sodium-Potassium-Exchanging ATPase/metabolism [MESH] |TRPV Cation Channels/antagonists & inhibitors/genetics/*metabolism [MESH] |Yolk Sac/cytology [MESH] |Zebrafish Proteins/antagonists & inhibitors/genetics/*metabolism [MESH]Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt si(epmc).pdf DeepDyve Pubget Overpricing