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10.1016/j.gene.2015.06.028 http://scihub22266oqcxt.onion/10.1016/j.gene.2015.06.028 C4496269!4496269!26074086     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       Gene 2015 ; 569 (1): 7-13 Nephropedia Template TP {{tp|p=26074086|t=2015. Nuclear Actions of Insulin-like Growth Factor Binding Protein-3 |pdf=|usr=}}{{26074086}} gab.com Text Nuclear Actions of Insulin-like Growth Factor Binding Protein-3 JO: Gene http://www.kidney.de/pget.php?&tw=1&pmid=26074086 #FOAvip In addition to its actions outside the cell, cellular uptake and nuclear import of insulin-like growth factor binding protein-3 (IGFBP-3) has been recognized for almost two decades, but knowledge of its nuclear actions has been slow to emerge. IGFBP-3 has a functional nuclear localization signal and interacts with the nuclear transport protein importin-?. Within the nucleus IGFBP-3 appears to have a role in transcriptional regulation. It can bind to the nuclear receptor, retinoid X receptor-? and several of its dimerization partners, including retinoic acid receptor, vitamin D receptor (VDR), and peroxisome proliferator-activated receptor-? (PPAR?). These interactions modulate the functions of these receptors, for example inhibiting VDR-dependent transcription in osteoblasts and PPAR?-dependent transcription in adipocytes. Nuclear IGFBP-3 can be detected by immunohistochemistry in cancer and other tissues, and its presence in the nucleus has been shown in many cell culture studies to be necessary for its pro-apoptotic effect, which may also involve interaction with the nuclear receptor Nur77, and export from the nucleus. IGFBP-3 is p53-inducible and in response to DNA damage, forms a complex with the epidermal growth factor receptor (EGFR), translocating to the nucleus to interact with DNA-dependent protein kinase. Inhibition of EGFR kinase activity or downregulation of IGFBP-3 can inhibit DNA double strand-break repair by nonhomologous endjoining. IGFBP-3 thus has the ability to influence many cell functions through its interactions with intranuclear pathways, but the importance of these interactions in vivo, and their potential to be targeted for therapeutic benefit, require further investigation. Twit Text FOAVip Nuclear Actions of Insulin-like Growth Factor Binding Protein-3 ????Gene http://www.kidney.de/pget.php?&tw=1&pmid=26074086 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26074086 #FOAvip English Wikipedia <ref>{{Cite pmid|26074086}}</ref> Nuclear Actions of Insulin-like Growth Factor Binding Protein-3 #MMPMID26074086 Baxter RC Gene 2015[Sep]; 569 (1): 7-13 PMID26074086show ga In addition to its actions outside the cell, cellular uptake and nuclear import of insulin-like growth factor binding protein-3 (IGFBP-3) has been recognized for almost two decades, but knowledge of its nuclear actions has been slow to emerge. IGFBP-3 has a functional nuclear localization signal and interacts with the nuclear transport protein importin-?. Within the nucleus IGFBP-3 appears to have a role in transcriptional regulation. It can bind to the nuclear receptor, retinoid X receptor-? and several of its dimerization partners, including retinoic acid receptor, vitamin D receptor (VDR), and peroxisome proliferator-activated receptor-? (PPAR?). These interactions modulate the functions of these receptors, for example inhibiting VDR-dependent transcription in osteoblasts and PPAR?-dependent transcription in adipocytes. Nuclear IGFBP-3 can be detected by immunohistochemistry in cancer and other tissues, and its presence in the nucleus has been shown in many cell culture studies to be necessary for its pro-apoptotic effect, which may also involve interaction with the nuclear receptor Nur77, and export from the nucleus. IGFBP-3 is p53-inducible and in response to DNA damage, forms a complex with the epidermal growth factor receptor (EGFR), translocating to the nucleus to interact with DNA-dependent protein kinase. Inhibition of EGFR kinase activity or downregulation of IGFBP-3 can inhibit DNA double strand-break repair by nonhomologous endjoining. IGFBP-3 thus has the ability to influence many cell functions through its interactions with intranuclear pathways, but the importance of these interactions in vivo, and their potential to be targeted for therapeutic benefit, require further investigation. äNuclear Actions of Insulin-like Growth Factor Binding Protein-3 (epmc).pdf DeepDyve Pubget Overpricing