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== Function ==
== Function ==
'''Serine/Threonine-protein kinase''' (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity of the [[AMP-activated protein kinase]] (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop within AMPK and non AMPK members. The non AMPK family proteins that it phosphorylates are STRADA, [[PTEN]] and possibly [[p53]]/TP53. The AMPK family members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as an upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of [[PI3K]]/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref name="Uniprot" />.
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of  STK11, which is also stabilized by MO25 intracting with the STK11 activation loop.  (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/) STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443).  STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)
 
 
 


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