Akt1Phospho(pT450)(AKT1)antibody

Akt1Phospho(pT450)(AKT1)antibody

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上海希美生物科技有限公司

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Akt1 Phospho(pT450)(AKT1)antibody
Cat.#: 3188-1
Rabbit Monoclonal Antibody
Clone ID: EPR4157
Swiss Prot: P31749
Mol Weight: 60kDa
Size: 100ul

Description
Akt1/PKBa is a Serine/Threonine protein kinase whose kinase activity plays a key role in various cellular functions, including apoptosis, glycogen synthesis, and cell growth. Akt1/PKBa is activated by various growth and survival factors (1). Akt1/PKBa inhibits apoptosis by phosphorylating and inactivating several targets, including caspase-9 (2). Akt1/PKBa regulates glycogen synthesis by phosphorylating and inactivating glycogen synthase kinase-3a and b (3,4).

Recommended Applications
WB, IHC, IP

Applications and Recommended Dilution Factors
WB: 1:1,000 -10,000
IHC: 1:50 - 100
IP: 1:10 - 100

Species Reactivity
Human, Mouse, Rat

For Mouse, this antibody is recommended for WB only
Rat cross reactivity tested by western blot only

Products Data 

 

 

Western blot analysis on NIH/3T3 cell lysate using anti-Akt1 Phospho (pT450) RabMAb (cat. #3188-1). Cells were either (A) untreated or (B) treated with Lambda Phosphatase.
Immunohistochemical analysis of paraffin-embedded human breast carcinoma using anti-Akt1 Phospho (pT450) RabMAb (cat. #3188-1).

Specificity
A phospho specific peptide corresponding to residues surrounding threonine 450 of human Akt1 was used as an immunogen. This antibody only detects Akt1 phosphorylated at threonine 450.

Storage Condition and Buffer
Store at -20 °C. Buffer: 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA. Stable for 12 months from date of receipt.

Alternative Names
AKT1 antibody, AKT antibody, MGC99656 antibody, PKB antibody, PKB-ALPHA antibody, PRKBA antibody, RAC antibody, RAC-ALPHA antibody, RAC-alpha serine/threonine-protein kinase antibody, Proto-oncogene c-Akt antibody, RAC-PK-alpha antibody

Description References
1. Burgering, B.M. and P.J. Coffer.Nature 376: 599-602 (1995).
2. Cardone, M.H., et al. Science 282: 1318-1321 (1998).
3. Hajduch, E., et al. FEBS Lett. 492: 199-203 (2001).
4. Cross, D.A., et al. Nature 378: 785-789 (1995). 

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