mProX™ Human SGK2 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX485	Magic™ Human SGK2 in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HeLa

Target Classification

Kinase Cell Lines

Target Research Area

Cancer Research

Related Diseases

Retinitis Pigmentosa 19; Colorectal Cancer

Gene ID

Human:10110

UniProt ID

Human:Q9HBY8

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

SGK2 (serum glucocorticoid-regulated kinase-2) has various applications in different fields. In the context of ischemia-reperfusion injury, SGK2 has the potential to be therapeutically modulated to reduce the burden of diseases such as myocardial infarction and acute kidney injury. In microvillus inclusion disease, patient-derived enteroids have been used to develop therapeutic approaches, and SGK2 has been identified as a potential pathway involved in rescuing MVID cells. Additionally, SGK2 plays a role in the regulation of epithelial-mesenchymal transition and cancer stem cell phenotypes in hepatocellular carcinoma. Furthermore, a neuroprotective treatment for acute optic neuritis and multiple sclerosis, OCS-05, binds to SGK2, displaying neuroprotective activity. Overall, SGK2 has implications in the development of therapeutic approaches for various diseases and conditions.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Morgan Jones (Verified Customer)

How does SGK2 influence cancer cell behavior? Jan 01 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

SGK2 is involved in regulating the localization and stability of the oncoprotein PTOV1, affecting cell-cycle progression in cancer. Jan 01 2023

chat Casey Johnson (Verified Customer)

What is the role of SGK2 in brown/beige adipose tissue thermogenesis? Dec 16 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

SGK2 is induced by the β3 adrenergic receptor-cAMP-PKA-PGC-1α/NT-PGC-1α axis in brown/beige adipose tissue, although it is dispensable for cold-induced thermogenesis. Dec 16 2021

Published Data

Fig.1 A reduction in cell viability was observed as a consequence of the introduction of SGK2 shRNAs.

Inhibition of HeLa cell proliferation/viability was observed upon the application of SGK2 shRNAs, with the data being represented as the average ± standard deviation of results obtained from two independent experiments.

Ref: Zhou, Nannan, et al. "Lethality of PAK3 and SGK2 shRNAs to human papillomavirus positive cervical cancer cells is independent of PAK3 and SGK2 knockdown." PLoS One 10.1 (2015): e0117357.

Pubmed: 25615606

DOI: 10.1371/journal.pone.0117357

Research Highlights

S, Mahmood. "Serum Glucocorticoid-Regulated Kinase-1 in Ischemia-Reperfusion Injury; Blessing or Curse." Journal of Pharmacology and Experimental Therapeutics, 2023.
The serum-glucocorticoid-regulated kinase (SGK) family consists of three paralogs- SGK-1, SGK-2 and SGK-3, with SGK-1 being the most extensively studied. Its involvement in regulating cell survival and proliferation has led to the development of small-molecule inhibitors for certain types of cancer. Additionally, SGK-1 plays a crucial role in physiological processes such as renal solute transport and has been linked to the development of non-neoplastic conditions in major organs like the heart and kidney. The potential for therapeutic intervention of SGK-1 to mitigate diseases like myocardial infarction and acute kidney injury is promising. This review will outline the structure and function of the SGK family and specifically focus on the role of SGK-1 in pathologies related to ischemia-reperfusion injury in organs such as the heart and kidney. Given the critical involvement of the mitochondrial permeability transition pore in cell death and the pro-survival function of SGK-1, there is potential for beneficial therapeutic modulation in conditions associated with ischemia-reperfusion injury.
S, Mahmood. "Serum Glucocorticoid-Regulated Kinase-1 in Ischemia-Reperfusion Injury; Blessing or Curse." Journal of Pharmacology and Experimental Therapeutics, 2023.
Pubmed: 37770199 DOI: 10.1124/jpet.123.001846

Kalashyan, Meri. et al. "Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease." The Journal of clinical investigation, 2023.
Microvillus Inclusion Disease (MVID), a severe infantile disorder characterized by diarrhea, malabsorption, and acid/base instability, is caused by loss-of-function mutations in the motor protein myosin Vb (MYO5B). The study aimed to investigate the disease by developing human enteroids with different MYO5B variants. Multiplex immunofluorescence imaging of patient duodenal tissues revealed changes in brush border transporter localization. Functional analysis of electrolyte transport and the use of crofelemer, a chloride channel-blocking drug, were conducted. MVID enteroids also exhibited altered differentiation and maturation compared to healthy enteroids. Transcriptomic analysis identified potential pathways involved in rescuing MVID cells. These findings demonstrate the potential of patient-derived enteroids in developing therapeutic strategies for MVID.
Kalashyan, Meri. et al. "Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease." The Journal of clinical investigation, 2023.
Pubmed: 37643022 DOI: 10.1172/JCI169234