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CDK9 (C12F7) Rabbit mAb

商城價：登錄可見

品牌：CST/賽信通

貨號：2316T

規(guī) 格：

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商品名稱	規(guī)格	代理級別	價格	運費	供應商	購買
CDK9 (C12F7) Rabbit mAb 交貨周期:現貨	20 μl	經銷	登錄可見	-	北京敏泰元科技有限公司	- + 立即購買庫存：20
CST 2316T CDK9(C12F7) Rabbit mAb 交貨周期:部分現貨，期貨3-4周左右，優(yōu)質售后	20μl	經銷	登錄可見	-	上海優(yōu)寧維生物科技股份有限公司	- + 立即購買庫存：999

產品詳情

文獻引用

文獻圖片

實驗數據

應用：W, IP, IHC-P, IHC-F, IF-IC, F
P-TEFb is a general transcription factor that regulates transcription elongation through phosphorylation of the C-terminal tail domain (CTD) of RNA polymerase II (RNAP II). The P-TEFb complex is composed of a catalytic subunit, CDK9, and its regulatory cyclin partner, which can be cyclin T1, T2a, T2b or K (reviewed in 1,2). P-TEFb is recruited by the HIV Tat protein to allow transcriptional elongation, and subsequent replication of the viral genome. Inhibition of P-TEFb function therefore has potential for HIV therapy. CDK9 exists as two isoforms, an abundant 42 kDa isoform, and a less abundant 55 kDa isoform, which contains an amino-terminal extension (3). The two forms likely have distinct purposes based on differential expression during lymphocyte activation (4,5) and on their localization within the nucleus (5).Cyclin dependent kinases (CDKs) are activated in part by cyclin binding and by phosphorylation of a conserved threonine in the T-loop domain. Phosphorylation of CDK9 at the T-loop Thr186 by an unidentified nuclear kinase may be important in P-TEFb activation (6) and regulation of HIV transcription (7). Acetylation of CDK9 at Lys44 affects its ability to phosphorylate the RNAPII CTD (8).

Supporting Data

REACTIVITY	H M R Hm Mk B Dg
SENSITIVITY	Endogenous
MW (kDa)	42, 55
Source/Isotype	Rabbit

Application Key:

W-Western
IP-Immunoprecipitation
IHC-Immunohistochemistry
ChIP-Chromatin Immunoprecipitation
IF-Immunofluorescence
F-Flow Cytometry
E-P-ELISA-Peptide

Species Cross-Reactivity Key:

H-Human
M-Mouse
R-Rat
Hm-Hamster
Mk-Monkey
Vir-Virus
Mi-Mink
C-Chicken
Dm-D. melanogaster
X-Xenopus
Z-Zebrafish
B-Bovine
Dg-Dog
Pg-Pig
Sc-S. cerevisiae
Ce-C. elegans
Hr-Horse
All-All Species Expected

Product Usage Information

Application	Dilution
Western Blotting	1:1000
Immunoprecipitation	1:100
Immunohistochemistry (Paraffin)	1:200
Immunohistochemistry (Frozen)	1:200
Immunofluorescence (Immunocytochemistry)	1:100
Flow Cytometry	1:200

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 μg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

Specificity / Sensitivity

CDK9 (C12F7) Rabbit mAb detects endogenous levels of total CDK9 protein, both 42 kDa and 55 kDa isoforms.

Species Reactivity:

Human, Mouse, Rat, Hamster, Monkey, Bovine, Dog

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human CDK9.

Background

P-TEFb is a general transcription factor that regulates transcription elongation through phosphorylation of the C-terminal tail domain (CTD) of RNA polymerase II (RNAP II). The P-TEFb complex is composed of a catalytic subunit, CDK9, and its regulatory cyclin partner, which can be cyclin T1, T2a, T2b or K (reviewed in 1,2). P-TEFb is recruited by the HIV Tat protein to allow transcriptional elongation, and subsequent replication of the viral genome. Inhibition of P-TEFb function therefore has potential for HIV therapy. CDK9 exists as two isoforms, an abundant 42 kDa isoform, and a less abundant 55 kDa isoform, which contains an amino-terminal extension (3). The two forms likely have distinct purposes based on differential expression during lymphocyte activation (4,5) and on their localization within the nucleus (5).

Cyclin dependent kinases (CDKs) are activated in part by cyclin binding and by phosphorylation of a conserved threonine in the T-loop domain. Phosphorylation of CDK9 at the T-loop Thr186 by an unidentified nuclear kinase may be important in P-TEFb activation (6) and regulation of HIV transcription (7). Acetylation of CDK9 at Lys44 affects its ability to phosphorylate the RNAPII CTD (8).

Rice, A.P. and Herrmann, C.H. (2003) Curr HIV Res 1, 395-404.
De Falco, G. and Giordano, A. (2002) Cancer Biol Ther 1, 342-7.
Shore, S.M. et al. (2003) Gene 307, 175-82.
Shore, S.M. et al. (2005) Gene 350, 51-8.
Liu, H. and Herrmann, C.H. (2005) J Cell Physiol 203, 251-60.
Chen, R. et al. (2004) J Biol Chem 279, 4153-60.
Ammosova, T. et al. (2005) Retrovirology 2, 47.
Fu, J. et al. (2007) Mol Cell Biol 27, 4641-51.

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