SGK3 Antibody [D18P23] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Lane 1: MCF7, Lane 2: COS-7, Lane 3: COLO 205

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse, Rat, Monkey

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
61 kDa

Datasheet & SDS

Biological Description

Specificity
SGK3 Antibody [D18P23] detects endogenous levels of total SGK3 protein.

Clone
D18P23

Synonym(s)
Serine/threonine-protein kinase Sgk3; Cytokine-independent survival kinase; Serum/glucocorticoid-regulated kinase 3; Serum/glucocorticoid-regulated kinase-like; SGK3; CISK; SGKL

Background
SGK3 (serum- and glucocorticoid-inducible kinase 3), a member of the SGK subfamily within the AGC kinase group and closely related to Akt, serves as an alternative effector in PI3K signaling, particularly in contexts where canonical Akt activation is compromised. It possesses a phox homology (PX) domain that uniquely binds phosphatidylinositol-3-phosphate (PI3P) on endosomes, alongside a kinase domain activated by sequential phosphorylation. Growth factors like IGF1 trigger SGK3 activation through dual Class 1 and Class 3 PI3K pathways: Class 1 PI3K generates PI(3,4,5)P3 that SHIP2 converts to PI3P for PX-domain recruitment, while mTORC2 phosphorylates the hydrophobic motif at Ser422 to prime T-loop Thr320 phosphorylation by PDK1, inducing a conformational shift that unlocks catalytic activity; concurrently, Class 3 PI3K (hVps34) directly produces PI3P via the UV-RAG complex, ensuring robust endosomal localization even when Class 1 PI3K is inhibited. Activated SGK3 then phosphorylates downstream targets like NDRG1 to promote its FBXW7-mediated degradation, enhancing cell migration and anchorage-independent growth, while sustaining glycogen synthase kinase-3 inhibition and FOXO3a nuclear exclusion to favor survival and proliferation. This pathway substitutes for Akt in PIK3CA-mutant breast and liver cancers, driving tumorigenesis through INPP4B-dependent PI3P accumulation, and physiologically regulates neuronal ion transport, renal sodium reabsorption, and metabolic adaptation to stress. Upregulation confers therapy resistance in PTEN-low cancers, while knockout impairs folliculogenesis and glucose homeostasis.

Background

SGK3 (serum- and glucocorticoid-inducible kinase 3), a member of the SGK subfamily within the AGC kinase group and closely related to Akt, serves as an alternative effector in PI3K signaling, particularly in contexts where canonical Akt activation is compromised. It possesses a phox homology (PX) domain that uniquely binds phosphatidylinositol-3-phosphate (PI3P) on endosomes, alongside a kinase domain activated by sequential phosphorylation. Growth factors like IGF1 trigger SGK3 activation through dual Class 1 and Class 3 PI3K pathways: Class 1 PI3K generates PI(3,4,5)P3 that SHIP2 converts to PI3P for PX-domain recruitment, while mTORC2 phosphorylates the hydrophobic motif at Ser422 to prime T-loop Thr320 phosphorylation by PDK1, inducing a conformational shift that unlocks catalytic activity; concurrently, Class 3 PI3K (hVps34) directly produces PI3P via the UV-RAG complex, ensuring robust endosomal localization even when Class 1 PI3K is inhibited. Activated SGK3 then phosphorylates downstream targets like NDRG1 to promote its FBXW7-mediated degradation, enhancing cell migration and anchorage-independent growth, while sustaining glycogen synthase kinase-3 inhibition and FOXO3a nuclear exclusion to favor survival and proliferation. This pathway substitutes for Akt in PIK3CA-mutant breast and liver cancers, driving tumorigenesis through INPP4B-dependent PI3P accumulation, and physiologically regulates neuronal ion transport, renal sodium reabsorption, and metabolic adaptation to stress. Upregulation confers therapy resistance in PTEN-low cancers, while knockout impairs folliculogenesis and glucose homeostasis.

References
https://pubmed.ncbi.nlm.nih.gov/25458846/ https://pubmed.ncbi.nlm.nih.gov/29150437/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%