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AKT1 Monoclonal Antibody_货号:E-AB-22211_单克隆抗体
AKT1 Monoclonal Antibody
WB;IHC-p
Mouse
Human
12个月
E-AB-22211
科研级别
999
武汉伊莱瑞特生物科技股份有限公司
Unconjugated
Monoclonal
Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles.
液体
IgG
120μL/60μL/20μL
规格: | 120μL | 产品价格: | ¥2310.0 |
---|---|---|---|
规格: | 60μL | 产品价格: | ¥1420.0 |
规格: | 20μL | 产品价格: | ¥580.0 |
Verified Samples |
Verified Samples in WB:PC-3
Verified Samples in IHC:Human lung carcinoma,Human breast carcinoma |
Dilution |
WB 1:1000-2000, IHC 1:100-200
|
Clonality |
Monoclonal
|
Isotype |
IgG
|
Immunogen |
Synthetic Peptide of AKT
|
Abbre |
AKT1
|
Synonyms |
AKT 1;AKT;AKT1;AKT1;MGC99656;PKB;PKB-ALPHA;PRKBA;Protein Kinase B Alpha;Protein kinase B;Proto-oncogene c-Akt;RAC Alpha;RAC;RAC-alpha serine/threonine-protein kinase;RAC-PK-alpha抗体
|
Swissprot |
P31749
|
Observed MW |
60kDa
|
Cellular Localization |
Cytoplasm. Nucleus. Cell membrane. Nucleus after activation by integrin-linked protein kinase 1 (ILK1). Nuclear translocation is enhanced by interaction with TCL1A. Phosphorylation on Tyr-176 by TNK2 results in its localization to the cell membrane where it is targeted for further phosphorylations on Thr-308 and Ser-473 leading to its activation and the activated form translocates to the nucleus.
|
Tissue Specificity |
Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.
|
Concentration |
1 mg/mL
|
Storage |
Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles.
|
Buffer |
PBS with 0.02% sodium azide, 0.5% protective protein and 50% glycerol, pH7.4
|
Purification Method |
Protein A purification
|
Research Areas |
Cancer; Epigenetics and Nuclear Signaling; Metabolism; Signal Transduction
|
Clone No. |
Clone:1H2
|
Conjugation |
Unconjugated
|
Background |
The serine-threonine protein kinase AKT1 is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery.
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