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10.18632/oncotarget.13099 http://scihub22266oqcxt.onion/10.18632/oncotarget.13099 C5348359!5348359!27825129     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27825129&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 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (49): 80842-54 Nephropedia Template TP {{tp|p=27825129|t=2016. Late-stage inhibition of autophagy enhances calreticulin surface exposure |pdf=|usr=}}{{27825129}} gab.com Text Late-stage inhibition of autophagy enhances calreticulin surface exposure JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27825129 #FOAvip Calreticulin (CRT) exposure on the cell surface is essential for inducing immunogenic cell death by chemotherapy. Recent studies have shown conflicting effects of chemotherapy-induced autophagy on CRT exposure in cancer cells. Our data revealed that surface-exposed CRT (Ecto-CRT) emission was attenuated by inhibition of autophagy at early stages; however, inhibition of autophagy at late stages resulted in increased Ecto-CRT. Furthermore, neither autophagy activation nor endoplasmic reticulum (ER) stress induction alone was sufficient for CRT surface exposure. Moreover, chemotherapeutic agents that only activated autophagy without inducing ER stress could not increase Ecto-CRT; therefore, combined use of an autophagy activator and ER stress inducer could effectively promote CRT translocation to the plasma membrane. Together, our results highlight the potential of the combined use of ER stress inducers and autophagy late-stage inhibitors to reestablish and strengthen both the CRT exposure and immunogenicity of chemotherapeutic agents induced death cells. Twit Text FOAVip Late-stage inhibition of autophagy enhances calreticulin surface exposure ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27825129 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27825129 #FOAvip English Wikipedia <ref>{{Cite pmid|27825129}}</ref> Late-stage inhibition of autophagy enhances calreticulin surface exposure #MMPMID27825129 Li DD; Xie B; Wu XJ; Li JJ; Ding Y; Wen XZ; Zhang X; Zhu SG; Liu W; Zhang XS; Peng RQ Oncotarget 2016[Dec]; 7 (49): 80842-54 PMID27825129show ga Calreticulin (CRT) exposure on the cell surface is essential for inducing immunogenic cell death by chemotherapy. Recent studies have shown conflicting effects of chemotherapy-induced autophagy on CRT exposure in cancer cells. Our data revealed that surface-exposed CRT (Ecto-CRT) emission was attenuated by inhibition of autophagy at early stages; however, inhibition of autophagy at late stages resulted in increased Ecto-CRT. Furthermore, neither autophagy activation nor endoplasmic reticulum (ER) stress induction alone was sufficient for CRT surface exposure. Moreover, chemotherapeutic agents that only activated autophagy without inducing ER stress could not increase Ecto-CRT; therefore, combined use of an autophagy activator and ER stress inducer could effectively promote CRT translocation to the plasma membrane. Together, our results highlight the potential of the combined use of ER stress inducers and autophagy late-stage inhibitors to reestablish and strengthen both the CRT exposure and immunogenicity of chemotherapeutic agents induced death cells. äLate-stage inhibition of autophagy enhances calreticulin surface expos(epmc).pdf DeepDyve Pubget Overpricing