CDK9 Antibody

說明書

中文名稱：

CDK9兔多克隆抗體
貨號：

CSB-PA005079GA01HU
規格：

￥3,900
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

Uniprot No.：

P50750
基因名：

CDK9
別名：

C-2K antibody; CDC2 related kinase antibody; CDC2L4 antibody; Cdk 9 antibody; Cdk9 antibody; CDK9_HUMAN antibody; Cell division cycle 2-like protein kinase 4 antibody; Cell division protein kinase 9 antibody; CTK1 antibody; Cyclin dependent kinase 9 antibody; Cyclin-dependent kinase 9 antibody; PITALRE antibody; Serine/threonine-protein kinase PITALRE antibody; TAK antibody; Tat associated kinase complex catalytic subunit antibody
宿主：

Rabbit
反應種屬：

Human,Mouse,Rat
免疫原：

Human CDK9
免疫原種屬：

Homo sapiens (Human)
抗體亞型：

IgG
純化方式：

Antigen Affinity Purified
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

PBS with 0.1% Sodium Azide, 50% Glycerol, pH 7.3. -20°C, Avoid freeze / thaw cycles.
產品提供形式：

Liquid
應用范圍：

ELISA,WB,IHC
Protocols：

ELISA Protocol
Western Blotting (WB) Protocol
Immunohistochemistry (IHC) Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase pair (CDK9/cyclin-T) complex, also called positive transcription elongation factor b (P-TEFb), which facilitates the transition from abortive to productive elongation by phosphorylating the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAP II) POLR2A, SUPT5H and RDBP. This complex is inactive when in the 7SK snRNP complex form. Phosphorylates EP300, MYOD1, RPB1/POLR2A and AR and the negative elongation factors DSIF and NELF. Regulates cytokine inducible transcription networks by facilitating promoter recognition of target transcription factors (e.g. TNF-inducible RELA/p65 activation and IL-6-inducible STAT3 signaling). Promotes RNA synthesis in genetic programs for cell growth, differentiation and viral pathogenesis. P-TEFb is also involved in cotranscriptional histone modification, mRNA processing and mRNA export. Modulates a complex network of chromatin modifications including histone H2B monoubiquitination (H2Bub1), H3 lysine 4 trimethylation (H3K4me3) and H3K36me3; integrates phosphorylation during transcription with chromatin modifications to control co-transcriptional histone mRNA processing. The CDK9/cyclin-K complex has also a kinase activity towards CTD of RNAP II and can substitute for CDK9/cyclin-T P-TEFb in vitro. Replication stress response protein; the CDK9/cyclin-K complex is required for genome integrity maintenance, by promoting cell cycle recovery from replication arrest and limiting single-stranded DNA amount in response to replication stress, thus reducing the breakdown of stalled replication forks and avoiding DNA damage. In addition, probable function in DNA repair of isoform 2 via interaction with KU70/XRCC6. Promotes cardiac myocyte enlargement. RPB1/POLR2A phosphorylation on 'Ser-2' in CTD activates transcription. AR phosphorylation modulates AR transcription factor promoter selectivity and cell growth. DSIF and NELF phosphorylation promotes transcription by inhibiting their negative effect. The phosphorylation of MYOD1 enhances its transcriptional activity and thus promotes muscle differentiation.
基因功能參考文獻：
1. miR-613, as a tumour suppressor, involves in gastric cancer progression and metastasis by targeting CDK9 PMID: 28701053
2. GRIP1 is phosphorylated at an N-terminal serine cluster by cyclin-dependent kinase-9 (CDK9), which is recruited into GC-induced GR:GRIP1:CDK9 hetero-complexes, producing distinct GRE-specific GRIP1 phospho-isoforms. PMID: 29170386
3. Recent studies have highlighted the importance of CDK9 in many relevant pathologic processes, like cancer, cardiovascular diseases, and viral replication. PMID: 28722178
4. This shows that CDK9 stimulates release of paused polymerase and activates transcription by increasing the number of transcribing polymerases and thus the amount of mRNA synthesized per time. PMID: 28994650
5. miR-206 is remarkably downregulated and is inversely correlated with CDK9 level in HCC cells. It is evident that miR-206 functions as a tumor suppressor through blocking CDK9-related pathway to induce apoptosis and inhibit HCC cell proliferation. PMID: 28940993
6. this study shows role of CDK9 in oncogenic processes of esophageal adenocarcinoma PMID: 28404924
7. Cdk9 is a post-exposure drug target against human adenoviruses. PMID: 28434229
8. BRD4 and CDK9 have independent, coordinated roles in promoting the myofibroblast transition PMID: 28182006
9. RBPJ links MYC and transcriptional control through CDK9 in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH PMID: 27322055
10. Chemical degrader of BET bromodomain proteins, dBET6, led to the unexpected identification of BRD4 as master regulator of global transcription elongation in acute T-cell leukemia. BRD4 loss does not directly affect CDK9 localization. PMID: 28673542
11. H1 variant interphase phosphorylation is dynamically regulated in a site-specific and gene-specific fashion during pluripotent cell differentiation, and that enrichment of pS187-H1.4 at genes is positively related to their transcription. H1.4-S187 is likely to be a direct target of CDK9 during interphase, suggesting the possibility that this particular phosphorylation may contribute the release of paused RNA pol II PMID: 28539972
12. HSP90 downstream HSF1 gives positive feedback to the reactivation process through binding to cyclin-dependent kinase 9 (CDK9) and preventing it from undergoing degradation by the proteasome. PMID: 27799305
13. We could conclude that there are many small molecules that bind to CDK9, but their lack of selectivity against other CDKs do not allow them to get to the clinical use PMID: 26766294
14. Findings indicate that cyclin-dependent kinase 9 (CDK9) represent an important role for inflammation in the pathogenesis of atherosclerosis. PMID: 26636538
15. Studies indicate that CDK9 regulates the genetic transcription at the early-elongation checkpoint close to poly(A) sites just before a functional polyadenylated mRNA is produced. PMID: 26853452
16. Our findings suggest a potential role of CDK9 in the radiation response of head and neck squamous cell carcinoma cells PMID: 26573875
17. Systematic Determination of Human CDK9 Interactome Identifies Novel Functions in RNA Splicing Mediated by the DDX5 and DDX17 RNA Helicases PMID: 26209609
18. In vitro phosphorylation of pUL69 by CDK9 or pUL97 did not occur in a single site-specific manner, but at multiple sites. PMID: 26555090
19. miR-191 represses proliferation in primary human fibroblasts via targeting multiple proto-oncogenes, including CDK9, NOTCH2, and RPS6KA3. PMID: 25992613
20. Essential for MYC expreession increase upon CDK9 inhibition is that the bromodomain protein BRD4 captures P-TEFb from 7SK snRNP to deliver to target genes and also enhances CDK9's activity and resistance to inhibition. PMID: 26083714
21. Suggest up-regulation of CDK9 kinase activity and Mcl-1 stability contributes to the acquired resistance to cyclin-dependent kinase inhibitors in leukemia. PMID: 25596730
22. Transcription is effective if RELA recruits the positive transcription elongation factor b (P-TEFb) component CDK9 to a combined RELA/STAT3 binding site -50 to -20bp upstream of the start site of the IL-12p35 promoter PMID: 25931145
23. Thus, inhibition of CDK9 may represent an interesting approach as a cancer therapeutic target, especially in hematologic malignancies. PMID: 24688048
24. MicroRNA-874 inhibits cell proliferation and induces apoptosis in human breast cancer by targeting CDK9 PMID: 25281924
25. LDC000067 represents a promising lead for the development of clinically useful, highly specific CDK9 inhibitors. PMID: 24102143
26. Cyclin dependent kinase-9 mediated transcriptional de-regulation of cMYC as a critical determinant of endocrine-therapy resistance in breast cancers. PMID: 24309997
27. Cdk9 is a new modulator of glucocorticoid receptor action and gene expression. PMID: 24559102
28. The cdk9 promotes inhibition and phosphorylation of Mdm2 on Ser-395, thus preventing degradation of p53, a protein that is directly involved in promoting p53 ubiquitination. PMID: 23603988
29. the phosphorylation of CDK9 at Ser175 plays a critical role in altering the competitive binding of Tat and BRD4 to P-TEFb and provides an informative molecular marker for the identification of the transcriptionally active form of P-TEFb. PMID: 23658523
30. These data demonstrate a pivotal role of Cdk9 activity for coupling of RNAPII transcription with small nucleolar RNA production and ribosomal RNA processing. PMID: 23744076
31. These data indicate that transcription elongation plays a major role in RSV-induced ISG expression and is mediated by IRF3-dependent recruitment of activated CDK9. PMID: 23596302
32. Data indicate that second-generation drugs resembling the original mimetic were found targeting of Cavity 1 and Cavity 2 regions on CDK9. PMID: 23247501
33. Structural delineation of a CDK9 conformation in which the C-terminal tail is structured and folds over the ATP binding site. PMID: 22959624
34. Studies indicate that the super elongation complex (SEC) consisting of ELL, P-TEFb (CDK9) and MLL required for rapid transcriptional induction in the presence or absence of paused RNA polymerase II (Pol II). PMID: 22895430
35. CDK9 phosphorylates UBE2A and regulates UBE2A-mediated monoubiquitination of both H2B and PCNA. PMID: 22592529
36. siRNA-mediated inhibition of Cdk9 caused a shift from G 0/G 1 to G 2/M phase in human PC3 prostate cancer cell line. PMID: 22391209
37. Data propose that CDK9 activity is a key regulator of neutrophil lifespan, preventing apoptosis by maintaining levels of short lived anti-apoptotic proteins such as Mcl-1. PMID: 22276149
38. This study examined kinases and signaling pathways that influence Cdk9 T-loop phosphorylation. PMID: 21448926
39. The inhibition of CDK9, the kinase subunit of P-TEFb, inhibited AIRE-induced pre-mRNA splicing of these genes. PMID: 21724609
40. Data indicate that P276-00 rapidly and significantly down regulated both Cdk9 and Mcl-1 protein expression levels in a dose and time-dependent manner. PMID: 21216463
41. [review] The direct role of CDK9-cyclin K in pathways that maintain genome integrity in response to replication stress appear to be evolutionarily conserved. PMID: 21200140
42. identify UBR5 as a novel E3 ligase that regulates transcription and define an additional function of TFIIS in the regulation of CDK9. PMID: 21127351
43. Tat efficiently replaces HEXIM1 on the 7SK snRNA in vivo and it promotes the disassembly of the 7SK/HEXIM/P-TEFb negative transcriptional regulatory snRNP to augment the nuclear level of active P-TEFb. PMID: 20976203
44. CDK9 phosphorylation of AR S81 is an important step in regulating AR transcriptional activity and prostate cancer cell growth PMID: 20980437
45. These results reveal an unexpectedly direct role for CDK9-cyclin K in checkpoint pathways that maintain genome integrity in response to replication stress. PMID: 20930849
46. IL-10 inhibits TNF gene at a level of transcription through a mechanism targeting the stimulation of transcription elongation by cyclin-dependent kinase 9 PMID: 20805562
47. These results demonstrate that cdk9 is involved in Tat-induced HIV-1 LTR, MCP-1/CCL2 gene expression PMID: 20370601
48. these findings suggest that the 55K CDK9 protein may function in repair of DNA through an association with Ku70. PMID: 20493174
49. Data suggest that CDK8 plays an important coactivator role in thyroid hormone receptor (TR)-dependent transcription by promoting Pol II recruitment and activation at TR target gene promoters. PMID: 20231357
50. NPAT is essential for histone mRNA 3' end processing and recruits CDK9 to replication-dependent histone genes. PMID: 20190802
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相關疾病：

Chronic activation of CDK9 causes cardiac myocyte enlargement leading to cardiac hypertrophy, and confers predisposition to heart failure.
亞細胞定位：

Nucleus. Cytoplasm. Nucleus, PML body. Note=Accumulates on chromatin in response to replication stress. Complexed with CCNT1 in nuclear speckles, but uncomplexed form in the cytoplasm. The translocation from nucleus to cytoplasm is XPO1/CRM1-dependent. Associates with PML body when acetylated.
蛋白家族：

Protein kinase superfamily, CMGC Ser/Thr protein kinase family, CDC2/CDKX subfamily
組織特異性：

Ubiquitous.
數據庫鏈接：

HGNC: 1780

OMIM: 603251

KEGG: hsa:1025

STRING: 9606.ENSP00000362361

UniGene: Hs.150423

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