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10.3389/fendo.2020.597573 http://scihub22266oqcxt.onion/10.3389/fendo.2020.597573 33312162!7708378!33312162     free     free     free 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       Front+Endocrinol+(Lausanne) 2020 ; 11 (ä): 597573 Nephropedia Template TP {{tp|p=33312162|t=2020. Growth Hormone Receptor Regulation in Cancer and Chronic Diseases |pdf=|usr=}}{{33312162}} gab.com Text Growth Hormone Receptor Regulation in Cancer and Chronic Diseases JO: Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=33312162 #FOAvip The GHR signaling pathway plays important roles in growth, metabolism, cell cycle control, immunity, homeostatic processes, and chemoresistance via both the JAK/STAT and the SRC pathways. Dysregulation of GHR signaling is associated with various diseases and chronic conditions such as acromegaly, cancer, aging, metabolic disease, fibroses, inflammation and autoimmunity. Numerous studies entailing the GHR signaling pathway have been conducted for various cancers. Diverse factors mediate the up- or down-regulation of GHR signaling through post-translational modifications. Of the numerous modifications, ubiquitination and deubiquitination are prominent events. Ubiquitination by E3 ligase attaches ubiquitins to target proteins and induces proteasomal degradation or starts the sequence of events that leads to endocytosis and lysosomal degradation. In this review, we discuss the role of first line effectors that act directly on the GHR at the cell surface including ADAM17, JAK2, SRC family member Lyn, Ubc13/CHIP, proteasome, betaTrCP, CK2, STAT5b, and SOCS2. Activity of all, except JAK2, Lyn and STAT5b, counteract GHR signaling. Loss of their function increases the GH-induced signaling in favor of aging and certain chronic diseases, exemplified by increased lung cancer risk in case of a mutation in the SOCS2-GHR interaction site. Insight in their roles in GHR signaling can be applied for cancer and other therapeutic strategies. Twit Text FOAVip Growth Hormone Receptor Regulation in Cancer and Chronic Diseases ????Front Endocrinol (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=33312162 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33312162 #FOAvip English Wikipedia <ref>{{Cite pmid|33312162}}</ref> Growth Hormone Receptor Regulation in Cancer and Chronic Diseases #MMPMID33312162 Strous GJ; Almeida ADS; Putters J; Schantl J; Sedek M; Slotman JA; Nespital T; Hassink GC; Mol JA Front Endocrinol (Lausanne) 2020[]; 11 (ä): 597573 PMID33312162show ga The GHR signaling pathway plays important roles in growth, metabolism, cell cycle control, immunity, homeostatic processes, and chemoresistance via both the JAK/STAT and the SRC pathways. Dysregulation of GHR signaling is associated with various diseases and chronic conditions such as acromegaly, cancer, aging, metabolic disease, fibroses, inflammation and autoimmunity. Numerous studies entailing the GHR signaling pathway have been conducted for various cancers. Diverse factors mediate the up- or down-regulation of GHR signaling through post-translational modifications. Of the numerous modifications, ubiquitination and deubiquitination are prominent events. Ubiquitination by E3 ligase attaches ubiquitins to target proteins and induces proteasomal degradation or starts the sequence of events that leads to endocytosis and lysosomal degradation. In this review, we discuss the role of first line effectors that act directly on the GHR at the cell surface including ADAM17, JAK2, SRC family member Lyn, Ubc13/CHIP, proteasome, betaTrCP, CK2, STAT5b, and SOCS2. Activity of all, except JAK2, Lyn and STAT5b, counteract GHR signaling. Loss of their function increases the GH-induced signaling in favor of aging and certain chronic diseases, exemplified by increased lung cancer risk in case of a mutation in the SOCS2-GHR interaction site. Insight in their roles in GHR signaling can be applied for cancer and other therapeutic strategies. |*Chronic Disease[MESH] |*Gene Expression Regulation[MESH] |Human Growth Hormone/*metabolism[MESH] |Humans[MESH] |Neoplasms/metabolism/*pathology[MESH]Growth Hormone Receptor Regulation in Cancer and Chronic Diseases (epmc).pdf DeepDyve Pubget Overpricing