Necessary for efficient RNA polymerase II transcription elongation past template-encoded arresting sites. The arresting sites in DNA have the property of trapping a certain fraction of elongating RNA polymerases that pass through, resulting in locked ternary complexes. Cleavage of the nascent transcript by S-II allows the resumption of elongation from the new 3'-terminus. (updated: April 1, 2015)
The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.
No sequence conservation computed yet.
Total structural coverage: 48%
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The reference OMIM entry for this protein is 601425
Transcription elongation factor a, 1; tcea1
Tcea
Tfiis; tf2s
Sii
CLONING
Transcription elongation factors help RNA polymerase II (see
180660) to transcribe past blockages due to specific DNA sequences, DNA-binding proteins, and transcription-arresting drugs. Transcription elongation factors in humans fall into 2 classes: the SIII (see
600788)/TF2F (see
189968) class, members of which increase the average rate of RNA chain elongation (Aso et al., 1995); and the SII class, which releases RNA polymerase II from transcriptional arrest (Reines, 1994). Park et al. (1994) cloned and characterized a human gene encoding an SII-type elongation factor that they called TFIIS. The TFIIS gene produces a 2.5-kb transcript.
GENE FUNCTION
Thomas et al. (1998) addressed whether the intrinsic 3-prime to 5-prime nuclease activity of human RNA polymerase II (pol II) can proofread during transcription in vitro. In the presence of SII, a protein that stimulates the nuclease activity, pol II quantitatively removed misincorporated nucleotides from the nascent transcript during rapid chain extension. The basis of discrimination between the correct and incorrect base was the slow addition of the next nucleotide to the mismatched terminus. Incorporation of inosine monophosphate inhibited the next nucleotide addition by a similar magnitude as a mismatched base. Thomas et al. (1998) demonstrated that addition of SII to a transcription reaction dramatically altered the RNA base content, reflecting the stable incorporation of more 'correct' (GMP) and fewer 'incorrect' (IMP) nucleotides. In vivo transcription by RNA polymerase II takes place in the context of chromatin. Guermah et al. (2006) found that a purified, reconstituted RNA polymerase II system that sufficed for activator-dependent transcription on DNA templates was incapable of transcribing chromatin templates, even in the presence of factors that effected transcription in less-purified assay systems. Using a complementation and HeLa cell nuclear extract fractionation scheme, Guermah et al. (2006) identified and purified an activity, designated CTEA (chromatin transcription-enabling activity), that allowed for transcription through chromatin templates in a manner that was both activator and p300 (EP300;
602700)/acetyl-CoA dependent. CTEA acted primarily at the elongation step and enabled RNA polymerase II machinery to transcribe efficiently through several contiguously positioned nucleosomes. Guermah et al. (2006) identified the major functional component of CTEA as transcription elongation factor SII. SII was essential for productive transcription elongation, and its function at this step was dependent on p300-dependent acetylation. These synergistic transcriptional elongation activities were potentiated by HMGB2 (
163906). Astrom et al. (1999) showed that activation of PLAG1 (
603026) in salivary gland tumors (
181030) is not confined to adenomas with 8q12 abnormalities but is also found in tumors with a normal karyotype. They showed further that PLAG1 may be activated by cryptic rearrangements in cases with normal karyotypes, leading to fusions between PLAG1 and CTNNB1 (
116806) or the TCEA1 gene.
GENE STRUCTURE
Park et al. (1994) determined that the TCEA1 gene is 2.8 kb long and intronless.
MAPPING
DiMarco et al. (1996) designed PCR primers for the TCEA1 gene and mapped it to human chromosome 3 by analysis of human-rodent hybrid mapping panel. Further regionalization to chromosome 3p22-p21.3 was accomplished by fluorescence in sit ...
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Feb. 2, 2018: Protein entry updated
Automatic update: Uniprot description updated
Dec. 19, 2017: Protein entry updated
Automatic update: Uniprot description updated
March 16, 2016: Protein entry updated
Automatic update: OMIM entry 601425 was added.
Jan. 25, 2016: Protein entry updated
Automatic update: model status changed