产品名称
SUPT5H Rabbit Polyclonal Antibody
蛋白名称
Transcription elongation factor SPT5 (hSPT5) (DRB sensitivity-inducing factor 160 kDa subunit) (DSIF p160) (DRB sensitivity-inducing factor large subunit) (DSIF large subunit) (Tat-cotransactivator 1 protein) (Tat-CT1 protein)
存储缓冲液
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.
Human Gene Link
http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=6829
Human Swissprot No.
O00267
Human Swissprot Link
https://www.uniprot.org/uniprot/O00267
Mouse Gene Link
http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=20924
Mouse Swissprot No.
O55201
Mouse Swissprot Link
https://www.uniprot.org/uniprotkb/O55201/entry
特异性
This antibody detects endogenous levels of SUPT5H at Human, Mouse
运输及保存条件
-15°C to -25°C/1 year(Do not lower than -25°C)
组织表达
Ubiquitously expressed.
功能
Component of the DRB sensitivity-inducing factor complex (DSIF complex), which regulates mRNA processing and transcription elongation by RNA polymerase II. DSIF positively regulates mRNA capping by stimulating the mRNA guanylyltransferase activity of RNGTT/CAP1A. DSIF also acts cooperatively with the negative elongation factor complex (NELF complex) to enhance transcriptional pausing at sites proximal to the promoter. Transcriptional pausing may facilitate the assembly of an elongation competent RNA polymerase II complex. DSIF and NELF promote pausing by inhibition of the transcription elongation factor TFIIS/S-II. TFIIS/S-II binds to RNA polymerase II at transcription pause sites and stimulates the weak intrinsic nuclease activity of the enzyme. Cleavage of blocked transcripts by RNA polymerase II promotes the resumption of transcription from the new 3' terminus and may allow repeated attempts at transcription through natural pause sites. DSIF can also positively regulate transcriptional elongation and is required for the efficient activation of transcriptional elongation by the HIV-1 nuclear transcriptional activator, Tat. DSIF acts to suppress transcriptional pausing in transcripts derived from the HIV-1 LTR and blocks premature release of HIV-1 transcripts at terminator sequences.
