产品描述

来源:
Mouse
应用:
ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000, IF/ICC 1:200-1:1000, FCM 1:200-1:400
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat, Monkey
克隆:
Monoclonal [AFB1740]
特异性:
GSK3B antibody detects endogenous levels of total GSK3B.
RRID:
AB_2833764
引用格式: Affinity Biosciences Cat# BF0695, RRID:AB_2833764.
偶联:
Unconjugated.
纯化:
Affinity-chromatography.
保存:
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Glycogen Synthase Kinase 3 Beta; Glycogen synthase kinase-3 beta; GSK 3 beta; GSK-3 beta; GSK3B; GSK3B_HUMAN; GSK3beta isoform; Serine/threonine-protein kinase GSK3B;

抗原和靶标

免疫原:

Purified recombinant fragment of human GSK3B expressed in E. Coli.

基因/基因ID:
描述:
Glycogen synthase kinase 3 (GSK-3), a serine-threonine kinase with two isoforms (alpha and beta), was originally discovered as a key enzyme in glycogen metabolism. GSK-3 was subsequently shown to function in cell division, proliferation, motility and survival. GSK-3 plays a role in a number of pathological conditions including cancer and diabetes and is increasingly seen as an important component of neurological diseases. GSK-3 phosphorylates tau and presenilin-1, which are involved in the development of Alzheimer's disease. Both isoforms of GSK-3 are ubiquitously expressed, although particularly high levels of GSK-3beta are found in the brain where it is involved in synaptic plasticity, possibly via regulation of NMDA receptor trafficking. GSK-3 phosphorylates over 40 different substrates including signaling proteins, transcription factors and structural proteins, and is part of the signal transduction cascade of a large number of growth factors and cytokines. The activity of GSK is regulated by phosphorylation (Akt: Akt-mediated phosphorylation at Ser21 of GSK-3α and Ser9 of GSK-3beta, S6K, RSK, PKA and PKC), dephosphorylation (PP1 and PP2A), and by binding to protein complexes (with beta-catenin, axin, CK1 and the APC complex).

研究领域

· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Wnt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Hedgehog signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Hippo signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Endometrial cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Basal cell carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer.   (View pathway)

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Development > Axon guidance.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Melanogenesis.

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

文献引用

1). Autophagic Inhibition of Caveolin-1 by Compound Phyllanthus urinaria L. Activates Ubiquitination and Proteasome Degradation of β-catenin to Suppress Metastasis of Hepatitis B-Associated Hepatocellular Carcinoma. Frontiers in Pharmacology, 2021 (PubMed: 34168559) [IF=5.6]

Application: WB    Species: Human    Sample: HepG2-HBx cell

FIGURE 7 Cav-1 inhibition by CP activated the Akt/GSK3β-mediated proteasome degradation of β-catenin via ubiquitination activation. (A) Wound healing assay showed the gap widths and areas were decreased in the Cav-1-overexpression groups, while CP treatment attenuated the migration ability of HBV-associated cells. (B) Compared to vector control, CP attenuated the promotion effect of Cav-1 on EMT process of HBV-associated HCC. (C) Cav-1 increased β-catenin expression and activated Akt/GSK3β pathway. CP treatment attenuated the effect of Cav-1 on β-catenin expression and Akt/GSK3β pathway of HBV-associated HCC. (D) Immunofluorescence assay of β-catenin expression and distribution in the cases of high Cav-1 expression and CP treatment. (E) Compared with the vector group, accumulation of β-catenin was accelerated in Cav-1-overexpressed group in the presence of CP following MG132 treatment. (F) CP significantly enhanced ubiquitination of β-catenin in HepG2-HBx cell lines with or without Cav-1 overexpression. (G) Wound healing array showed that β-catenin knockdown partly abrogated the capacity of Cav-1 to promote migration in HepG2-HBx cell. All values represented the means ± SD (n = 3, *p < 0.05, **p < 0.01, ***p < 0.001, # p < 0.05, ## p < 0.01, ### p < 0.001).

2). Anemoside B4 alleviates arthritis pain via suppressing ferroptosis-mediated inflammation. Journal of cellular and molecular medicine, 2024 (PubMed: 38334255) [IF=5.3]

Application: WB    Species: Mouse    Sample:

FIGURE 5 (A) The molecular structure of AB4. (B–D) Molecular docking of AB4 with GSK‐3β. The modelled 3D structure of GSK‐3β docked with AB4 (B). The enlarged view of binding site in box (C). The interaction bonds of GSK‐3β with AB4 (D). Bonds showed as yellow dotted lines, and bond lengths were presented as numbers. (E) The titration between AB4 and GSK‐3β. The top panel presents typical calorimetric titration of AB4 with GSK‐3β at 25°C. The bottom panel shows the plots of the heat evolved (kcal) per mol of AB4 added corrected for the heat of with GSK‐3β, against the molar ratio of AB4 to GSK‐3β. Data solid squares were fitted to a single set of the identical sites model, and the solid line represented the best fit. (F) Representative immunofluorescence staining images of GSK‐3β and Drp1 in the spinal dorsal horn of the control, CIA and CIA + AB4 groups. Scale bar = 20 μm. (G) Quantitative analysis of the fluorescence intensity of GSK‐3β and Drp1. (H, I) Western blot analysis and quantitative grey value analysis of pGSK‐3β‐Tyr216, GSK‐3β, pDrp1‐Ser616, pDrp1‐Ser637 and Drp1 level in the spinal cord of the control, CIA and CIA + AB4 groups. Data are presented as mean ± SD (n = 5). *p 

3). DEPDC1B-mediated USP5 deubiquitination of β-catenin promotes breast cancer metastasis by activating the wnt/β-catenin pathway. American Journal of Physiology-Cell Physiology, 2023 (PubMed: 37642235) [IF=5.0]

Application: WB    Species: Human    Sample: breast cancer cells

Figure 6. The expression of DEP domain-containing protein 1B (DEPDC1B) can activate the wnt/β-catenin signaling pathway. A: functional enrichment analysis of the results of protein spectrum identification. B: the results of KEGG analysis showed that the signal pathway related to the DEPDC1B interacting proteins. C and D: DEPDC1B is involved in the nuclear translocation of β-catenin. Hs578T cells (C) were transfected with negative control (NC) and DEPDC1B siRNA, MDA-MB-157 cells (D) were transfected with vector and DEPDC1B overexpression plasmids, and the expression of β-catenin was detected by immunofluorescence after 48 h. Scale bars, 20 μm. E: the results of the statistical analysis of C and D. Analysis between 2 groups was conducted by unpaired Student’s t test. *P < 0.05. F: the expression levels of wnt3a, phospho (p-)GSK-3β (ser9), GSK-3β, and β-catenin were detected by Western blot, and GAPDH was used as the internal control. G: Western blot results of the expression of DEPDC1B, wnt3a, and β-catenin in MDA-MB-157 cells transfected with DEPDC1B overexpression plasmid alone or in combination with XAV-939, with GAPDH as the internal control.

4). Effects of dexmedetomidine postconditioning on myocardial ischemia and the role of the PI3K/Akt-dependent signaling pathway in reperfusion injury. Molecular Medicine Reports, 2016 (PubMed: 27221008) [IF=3.4]

Application: WB    Species: rat    Sample:


5). Curcumin relieves oxaliplatin-induced neuropathic pain via reducing inflammation and activating antioxidant response. Cell biology international, 2024 (PubMed: 38480956) [IF=3.3]

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