SGK2
- Known as:
- SGK2
- Catalog number:
- 000335A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SGK2
Related genes to: SGK2
- Gene:
- SGK2 NIH gene
- Name:
- serum/glucocorticoid regulated kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-21
- Date modifiied:
- 2019-04-23
- Gene:
- SGK3 NIH gene
- Name:
- serum/glucocorticoid regulated kinase family member 3
- Previous symbol:
- SGK2, SGKL
- Synonyms:
- -
- Chromosome:
- 8q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-12
- Date modifiied:
- 2016-11-15
Related products to: SGK2
Related articles to: SGK2
- The family of serum-glucocorticoid-regulated kinase (SGK) consists of three paralogs, SGK-1, SGK-2, and SGK-3, with SGK-1 being the better studied. Indeed, recognition of the role of SGK-1 in regulation of cell survival and proliferation has led to introduction of a number of small-molecule inhibitors for some types of cancer. In addition, SGK-1 regulates major physiologic effects, such as renal solute transport, and contributes to the pathogenesis of non-neoplastic conditions involving major organs including the heart and the kidney. These observations raise the prospect for therapeutic modulation of SGK-1 to reduce the burden of such diseases as myocardial infarction and acute kidney injury. Following a brief description of the structure and function of SGK family of proteins, the present review is primarily focused on our current understanding of the role of SGK-1 in pathologies related to ischemia-reperfusion injury involving several organs (e.g., heart, kidney). The essential role of the mitochondrial permeability transition pore in cell death coupled with the pro-survival function of SGK-1 raise the prospect that its therapeutic modulation could beneficially impact conditions associated with ischemia-reperfusion injury. SIGNIFICANCE STATEMENT: Since the discovery of serum glucocorticoid-regulated kinase (SGK)-1, extensive research has unraveled its role in cancer biology and, thus, its therapeutic targeting. Increasingly, it is also becoming clear that SGK-1 is a major determinant of the outcome of ischemia-reperfusion injury to various organs. Thus, evaluation of existing information should help identify gaps in our current knowledge and also determine whether and how its therapeutic modulation could impact the outcome of ischemia-reperfusion injury. - Source: PubMed
Publication date: 2023/09/28
Mozaffari Mahmood S - Serum- and glucocorticoid-regulated kinases (SGKs) are members of the AGC family of serine/threonine kinases, consisting of three isoforms: SGK1, SGK2, and SGK3. SGK1 was initially cloned as a gene transcriptionally stimulated by serum and glucocorticoids in rat mammary tumor cells. It is upregulated in some cancers and downregulated in others. SGK1 increases tumor cell survival, adhesiveness, invasiveness, motility, and epithelial to mesenchymal transition. It stimulates tumor growth by mechanisms such as activation of K channels and Ca channels, Na/H exchanger, amino acid and glucose transporters, downregulation of Foxo3a and p53, and upregulation of β-catenin and NFκB. This chapter focuses on major aspects of SGK1 involvement in cancer, its use as biomarker as well as potential therapeutic target. - Source: PubMed
Publication date: 2022/05/12
Cicenas JonasMeskinyte-Kausiliene EditaJukna VigilijusRimkus ArnasSimkus JokubasSoderholm Diana - In mammalian females, oocytes are stored in the ovary and meiosis is arrested at the diplotene stage of prophase I. When females reach puberty oocytes are selectively recruited in cycles to grow, overcome the meiotic arrest, complete the first meiotic division and become mature (ready for fertilization). At a molecular level, the master regulator of prophase I arrest and meiotic resumption is the maturation-promoting factor (MPF) complex, formed by the active form of cyclin dependent kinase 1 (CDK1) and Cyclin B1. However, we still do not have complete information regarding the factors implicated in MPF activation. In this study we document that out of three mammalian serum-glucocorticoid kinase proteins (SGK1, SGK2, SGK3), mouse oocytes express only SGK1 with a phosphorylated (active) form dominantly localized in the nucleoplasm. Further, suppression of SGK1 activity in oocytes results in decreased CDK1 activation via the phosphatase cell division cycle 25B (CDC25B), consequently delaying or inhibiting nuclear envelope breakdown. Expression of exogenous constitutively active CDK1 can rescue the phenotype induced by SGK1 inhibition. These findings bring new insights into the molecular pathways acting upstream of MPF and a better understanding of meiotic resumption control by presenting a new key player SGK1 in mammalian oocytes. - Source: PubMed
Publication date: 2022/02/25
Del Llano EdgarIyyappan RajanAleshkina DariaMasek TomasDvoran MichalJiang ZongliangPospisek MartinKubelka MichalSusor Andrej - A hallmark of type 2 diabetes (T2D) is hepatic resistance to insulin's glucose-lowering effects. The serum- and glucocorticoid-regulated family of protein kinases (SGK) is activated downstream of mechanistic target of rapamycin complex 2 (mTORC2) in response to insulin in parallel to AKT. Surprisingly, despite an identical substrate recognition motif to AKT, which drives insulin sensitivity, pathological accumulation of SGK1 drives insulin resistance. Liver-specific Sgk1-knockout (Sgk1) mice display improved glucose tolerance and insulin sensitivity and are protected from hepatic steatosis when fed a high-fat diet. Sgk1 promotes insulin resistance by inactivating AMP-activated protein kinase (AMPK) via phosphorylation on inhibitory site AMPKα. We demonstrate that SGK1 is dominant among SGK family kinases in regulation of insulin sensitivity, as Sgk1, Sgk2, and Sgk3 triple-knockout mice have similar increases in hepatic insulin sensitivity. In aggregate, these data suggest that targeting hepatic SGK1 may have therapeutic potential in T2D. - Source: PubMed
Zhou BenZhang YuyaoLi SainanWu LianfengFejes-Toth GezaNaray-Fejes-Toth AnikoSoukas Alexander A - The serum- and glucocorticoid-regulated kinase (SGK) family consists of three isoforms (SGK1, SGK2, and SGK3) that have been implicated in the regulation of tumor growth, metastasis, autophagy, and epithelial ion transport. SGK1 and SGK3 play essential roles in protein kinase B (AKT or PKB)-independent phosphoinositide 3-kinases (PI3K)-mediated tumorigenesis, as evidenced by the significantly elevated expression levels of SGK1 and SGK3 in many cancers, including prostate cancer, colorectal carcinoma, estrogen-dependent breast cancer, and glioblastoma. Therefore, SGK is a potential target for anticancer therapy. A small kinase-focused library comprising 160 compounds was screened against SGK1 using a fluorescence polarization-based kinase assay that yielded a Z'-factor of 0.82. Among the 39 compounds obtained as initial hits in a primary screen, 12 compounds contained the thiazolidine-2,4-dione scaffold. The inhibitory mechanisms of the most potent hit, KMU010402, were further investigated using kinetic analyses, followed by determination of the inhibition constants for SGK1, SGK2, and SGK3. Molecular modeling was used to propose a potential binding mode of KMU010402 to SGK1. - Source: PubMed
Publication date: 2021/03/30
Kim JeongeunKim DongheeJung HyunhoLee JinhoHong Victor Sukbong