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10.1126/scisignal.aam8705 http://scihub22266oqcxt.onion/10.1126/scisignal.aam8705 C5914505!5914505!29295957     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 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       Sci+Signal 2018 ; 11 (511): ä Nephropedia Template TP {{tp|p=29295957|t=2018. The depalmitoylase APT1 directs the asymmetric partitioning of Notch and Wnt signaling during cell division |pdf=|usr=}}{{29295957}} gab.com Text The depalmitoylase APT1 directs the asymmetric partitioning of Notch and Wnt signaling during cell division JO: Sci Signal http://www.kidney.de/pget.php?&tw=1&pmid=29295957 #FOAvip Asymmetric cell division results in two distinctly fated daughter cells. A molecular hallmark of asymmetric division is the unequal partitioning of cell fate determinants. We have previously established that growth factor signaling promotes protein depalmitoylation to foster polarized protein localization, which in turns drives migration and metastasis. Here, we report protein palmitoylation as a key mechanism for the asymmetric partitioning of the cell fate determinants Numb and ?-catenin through the activity of the depalmitoylating enzyme APT1. Using point mutations, we show specific palmitoylated residues on Numb are required for asymmetric localization. By live-cell imaging, we show that reciprocal interactions between APT1 and the Rho-family GTPase CDC42 promote the asymmetric localization of Numb and ?-catenin to the plasma membrane. This in turn restricts Notch- and Wnt-responsive transcriptional activity to one daughter cell. Moreover, we show altering APT1 expression changes the transcriptional signatures of MDA-MB-231 triple receptor?negative breast cancer cells similarly to changes in Notch and ?-catenin?mediated Wnt signaling. We also show that loss of APT1 depletes a specific subpopulation of tumorigenic cells in colony formation assays. Together, our findings demonstrate that APT1-mediated depalmitoylation is a major mechanism of asymmetric cell division maintaining Notch and Wnt-associated protein dynamics, gene expression, and cellular functions. Twit Text FOAVip The depalmitoylase APT1 directs the asymmetric partitioning of Notch and Wnt signaling during cell division ????Sci Signal http://www.kidney.de/pget.php?&tw=1&pmid=29295957 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29295957 #FOAvip English Wikipedia <ref>{{Cite pmid|29295957}}</ref> The depalmitoylase APT1 directs the asymmetric partitioning of Notch and Wnt signaling during cell division #MMPMID29295957 Stypulkowski E; Asangani IA; Witze ES Sci Signal 2018[Jan]; 11 (511): ä PMID29295957show ga Asymmetric cell division results in two distinctly fated daughter cells. A molecular hallmark of asymmetric division is the unequal partitioning of cell fate determinants. We have previously established that growth factor signaling promotes protein depalmitoylation to foster polarized protein localization, which in turns drives migration and metastasis. Here, we report protein palmitoylation as a key mechanism for the asymmetric partitioning of the cell fate determinants Numb and ?-catenin through the activity of the depalmitoylating enzyme APT1. Using point mutations, we show specific palmitoylated residues on Numb are required for asymmetric localization. By live-cell imaging, we show that reciprocal interactions between APT1 and the Rho-family GTPase CDC42 promote the asymmetric localization of Numb and ?-catenin to the plasma membrane. This in turn restricts Notch- and Wnt-responsive transcriptional activity to one daughter cell. Moreover, we show altering APT1 expression changes the transcriptional signatures of MDA-MB-231 triple receptor?negative breast cancer cells similarly to changes in Notch and ?-catenin?mediated Wnt signaling. We also show that loss of APT1 depletes a specific subpopulation of tumorigenic cells in colony formation assays. Together, our findings demonstrate that APT1-mediated depalmitoylation is a major mechanism of asymmetric cell division maintaining Notch and Wnt-associated protein dynamics, gene expression, and cellular functions. äThe depalmitoylase APT1 directs the asymmetric partitioning of Notch a(epmc).pdf DeepDyve Pubget Overpricing