CCNT1 Antibody | anti-CCNT1 antibody

CCNT1 Antibody

Cat. Num. AAA8516257

• Gene Names: CCNT1; CCNT; CYCT1; HIVE1
• Reactivity: Human, Mouse, Rat
• Applications: Western Blot, Immunohistochemistry
• Purity: Immunogen affinity purified
• Synonyms: CCNT1; CCNT1 Antibody; CCNT; CYCT1; HIVE1; Cyclin T1; anti-CCNT1 antibody

• Reactivity: Human, Mouse, Rat
• Specificity: CCNT1 Antibody detects endogenous levels of total CCNT1
• Purity/Purification: Immunogen affinity purified
• Form/Format: In phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
• Sequence Length: 726

• Applicable Applications for anti-CCNT1 antibody: Western Blot (WB), Immunohistochemistry (IHC)
• Application Notes: WB: 1:500-1:2000; IHC: 1:50-1:200
• Immunogen: A synthetic peptide of human CCNT1
• Preparation and Storage: Store at-20 degree C for 1 year

Western Blot (WB)

(Western blot analysis of extracts of K562cell lines, using CCNT1 antibody.)

Related Product Information for anti-CCNT1 antibody

Positive transcription elongation factor (P-TEFb) is a heterodimer composed of cyclin T proteins and CDK9. P-TEFb plays a critical role in the transition of the RNA polymerase II (RNAPII) machinery from transcription initiation to elongation (1). At some genes during transcription initiation, RNAPII moves approximately 50 nucleotides away from the transcription start site into the gene where it then pauses and awaits signaling for the formation of a productive transcription elongation complex (1, 2). The release of this promoter proximal pausing of RNAPII is signaled by phosphorylation of the C-terminal domain (CTD) within the largest subunit of RNAPII at Ser2 of the heptapeptide repeat sequence by P-TEFb (3). This phosphorylation event is important for the recruitment of mRNA processing factors and chromatin modifiers that are necessary for proper gene expression (4, 5). P-TEFb also promotes transcription elongation by phosphorylating DSIF (DRB-induced stimulating factor) and NELF (negative elongation factor), two negative elongation factors that retain RNAPII at the promoter proximal region of genes to initiate transcription elongation (6, 7).

NCBI and Uniprot Product Information

• NCBI GI #: 17978466
• NCBI GeneID: 904
• NCBI Accession #: NP_001231.2
• NCBI GenBank Nucleotide #: NM_001240.3
• UniProt Accession #: O60563; O60581; A9XU13; E7EX76
• Molecular Weight: 81kDa
• NCBI Official Full Name: cyclin-T1 isoform a
• NCBI Official Synonym Full Names: cyclin T1
• NCBI Official Symbol: CCNT1
• NCBI Official Synonym Symbols: CCNT; CYCT1; HIVE1
• NCBI Protein Information: cyclin-T1
• UniProt Protein Name: Cyclin-T1
• Protein Family: Cyclin
• UniProt Gene Name: CCNT1
• UniProt Synonym Gene Names: CycT1; Cyclin-T

NCBI Description

This gene encodes a member of the highly conserved cyclin C subfamily. The encoded protein tightly associates with cyclin-dependent kinase 9, and is a major subunit of positive transcription elongation factor b (p-TEFb). In humans, there are multiple forms of positive transcription elongation factor b, which may include one of several different cyclins along with cyclin-dependent kinase 9. The complex containing the encoded cyclin and cyclin-dependent kinase 9 acts as a cofactor of human immunodeficiency virus type 1 (HIV-1) Tat protein, and is both necessary and sufficient for full activation of viral transcription. This cyclin and its kinase partner are also involved in triggering transcript elongation through phosphorylation of the carboxy-terminal domain of the largest RNA polymerase II subunit. Overexpression of this gene is implicated in tumor growth. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Apr 2013]

Uniprot Description

Regulatory subunit of the cyclin-dependent kinase pair (CDK9/cyclin-T1) complex, also called positive transcription elongation factor B (P-TEFb), which is proposed to facilitate the transition from abortive to productive elongation by phosphorylating the CTD (carboxy-terminal domain) of the large subunit of RNA polymerase II (RNA Pol II).