SUPT5H Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, E |
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Primary Accession | O00267 |
Other Accession | O55201, Q5ZI08, NP_001104490.1, NP_001124297.1, NP_001124296.1 |
Reactivity | Human |
Predicted | Chicken, Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 121000 Da |
Antigen Region | 395-424 aa |
Gene ID | 6829 |
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Other Names | 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, SUPT5H, SPT5, SPT5H |
Target/Specificity | This SUPT5H antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 395-424 amino acids from the Central region of human SUPT5H. |
Dilution | WB~~1:1000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | SUPT5H Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | SUPT5H |
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Synonyms | SPT5, SPT5H |
Function | 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. |
Cellular Location | Nucleus. |
Tissue Location | Ubiquitously expressed. |

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Background
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.
References
Wenzel, S., et al. Biochem. J. 425(2):373-380(2010)
Chen, Y., et al. Genes Dev. 23(23):2765-2777(2009)
Komori, T., et al. Genes Cells 14(3):343-354(2009)
Chen, H., et al. PLoS ONE 4 (9), E6918 (2009) :
Amir-Zilberstein, L., et al. J. Biol. Chem. 283(3):1317-1323(2008)

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