Envelope glycoprotein gp160 is single-pass type I membrane protein. The mature envelope protein (Env) consists of a homotrimer of non-covalently associated gp120-gp41 heterodimers. It is cleaved into the following 2 chains: glycoprotein 120 and transmembrane protein gp41. The resulting complex protrudes from the virus surface as a spike. The 17 amino acids long immunosuppressive region is present in many retroviral envelope proteins. Synthetic peptides derived from this relatively conserved sequence inhibit immune function in vitro and in vivo.
14-3-3 beta / YWHAB is a member of the 14-3-3 proteins family. 14-3-3 proteins are a group of highly conserved proteins that are involved in many vital cellular processes such as metabolism, protein trafficking, signal transduction, apoptosis and cell cycle regulation. 14-3-3 proteins are mainly localized in the synapses and neuronal cytoplasm, and seven isoforms have been identified in mammals. This family of proteins was initially identified as adaptor proteins which bind to phosphoserine-containing motifs. Binding motifs and potential functions of 14-3-3 proteins are now recognized to have a wide range of functional relevance. 14-3-3 beta / YWHAB is found in both plants and mammals, and this protein is 100% identical to the mouse ortholog. 14-3-3 beta / YWHAB interacts with CDC25 phosphatases, RAF1 and IRS1 proteins, suggesting its role in diverse biochemical activities related to signal transduction, such as cell division and regulation of insulin sensitivity. 14-3-3 beta / YWHAB has also been implicated in the pathogenesis of small cell lung cancer. 14-3-3 beta / YWHAB binding negatively regulates RSK1 activity to maintain signal specificity and that association/dissociation of the 14-3-3beta-RSK1 complex is likely to be important for mitogen-mediated RSK1 activation.
YWHAE; also known as 14-3-3 epsilon; mediate signal transduction by binding to phosphoserine-containing proteins. 14-3-3 epsilon / YWHAE is a member of the 14-3-3 proteins family. 14-3-3 proteins are a group of highly conserved proteins that are involved in many vital cellular processes such as metabolism; protein trafficking; signal transduction; apoptosis and cell cycle regulation. 14-3-3 proteins are mainly localized in the synapses and neuronal cytoplasm; and seven isoforms have been identified in mammals. This family of proteins was initially identified as adaptor proteins which bind to phosphoserine-containing motifs. Binding motifs and potential functions of 14-3-3 proteins are now recognized to have a wide range of functional relevance. 14-3-3 epsilon / YWHAE is found in both plants and mammals; and this protein is 100% identical to the mouse ortholog. YWHAE interacts with CDC25 phosphatases; RAF1 and IRS1 proteins; suggesting its role in diverse biochemical activities related to signal transduction; such as cell division and regulation of insulin sensitivity. It has also been implicated in the pathogenesis of small cell lung cancer. 14-3-3 epsilon / YWHAE is implicated in the regulation of a large spectrum of both general and specialized signaling pathways. 14-3-3 epsilon / YWHAE Binds to a large number of partners; usually by recognition of a phosphoserine or phosphothreonine motif. This Binding generally results in the modulation of the activity of the binding partner.
14-3-3 Protein Epsilon acts as an adapter protein implicated in the regulation of a large spectrum of both general and specialized signaling pathways. 14-3-3 protein epsilon binds to a large number of partners, usually by recognition of a phophoserine or phosphothreonine motif. Binding generally results in the modulation of the activity of the binding partner.
YWHAH, the gene encoding the 14-3-3eta isoform, is highly expressed in retinal ganglion cells (RGC). YWHAH is a positional and functional candidate gene for both schizophrenia and bipolar disorder (BP). It is located on chromosome 22q12.3, a region which has been implicated by linkage studies in both BP and schizophrenia.
14-3-3 protein sigma (YWHAS); also known as stratifin (SFN) and epithelial cell marker protein 1; is a member of the14-3-3 proteins which are a family of conserved regulatory molecules expressed in all eukaryotic cells. The name 14-3-3 refers to the particular elution and migration pattern of these proteins on DEAE-cellulose chromatography and starch-gel electrophoresis. The 14-3-3 proteins eluted in the 14th fraction of bovine brain homogenate and were found on positions 3.3 of subsequent electrophoresis. There are seven genes that encode 14-3-3s in most mammals. 14-3-3 proteins have been identified as adapter proteins implicated in the regulation of a large spectrum of both general and specialized signaling pathway. More than 100 signaling proteins have been reported as 14-3-3 ligands including kinases; phosphatases; and transmembrane receptors; and the binding generally results in the modulation of the activity of the binding partner. YWHAE exists as a homodimer and present mainly in tissues enriched in stratified squamous keratinising epithelium. YWHAS has been repoted to interact with KRT17 and GAB2; and may regulate protein synthesis and epithelial cell growth by stimulating Akt/mTOR pathway upon binding to KRT17. Additionally; YWHAS (SFN) may also act as a p53-regulated inhibitor of G2/M progression.
G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors. GRK5 contains oneAGC-kinase C-terminal domain, oneprotein kinase domain and oneRGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.
15-hydroxyprostaglandin dehydrogenase [NAD(+)], also known as Prostaglandin dehydrogenase 1, 15-PGDH, HPGD and PGDH1, belongs to the short-chain dehydrogenases/reductases (SDR) family. HPGD localizes to the cytoplasm and can be found in colon epithelium, existing as a homodimer. HPGD catalyzes the NAD-dependent dehydrogenation of lipoxin A4 to form 15-oxo-lipoxin A4. HPGD is down-regulated by cortisol, dexamethasone and betamethasone, up-regulated by TGFB1. HPGD inhibits in vivo proliferation of colon cancer cells. HPGD is the key enzyme for the inactivation of prostaglandins, and thus regulates processes such as inflammation or proliferation.
15-hydroxyprostaglandin dehydrogenase [NAD+], also known as Prostaglandin dehydrogenase 1, HPGD, and PGDH1, is a member of the short-chain dehydrogenases/reductases (SDR) family. Prostaglandins (PGs) play a key role in the onset of labor inmany species and regulate uterine contractility and cervicaldilatation. Therefore, the regulation of prostaglandin outputby PG synthesizing and metabolizing enzymes in the human myometrium may determine uterine activitypatterns in human labor both at preterm and at term. Prostaglandin dehydrogenase (PGDH) metabolizes prostaglandins (PGs) to render them inactive. HPGD is down-regulated by cortisol, dexamethasone and betamethasone and down-regulated in colon cancer. It is up-regulated by TGFB1. HPGD contributes to the regulation of events that are under the control of prostaglandin levels. HPGD catalyzes the NAD-dependent dehydrogenation of lipoxin A4 to form 15-oxo-lipoxin A4. and inhibits in vivo proliferation of colon cancer cells. Defects in HPGD are the cause of primary hypertrophic osteoathropathy autosomal recessive (PHOAR), cranioosteoarthropathy (COA),and isolated congenital nail clubbing.
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