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Epub Aug Epub Nov Epub Feb Epub Jun 3. It is useful for tracking sequence updates. The algorithm is described in the ISO standard. Note: No experimental confirmation available. Mass Da : 84, Mass Da : 58, Checksum: i 6CB5E6D Mass Da : 49, Mass Da : 92, Checksum: i 75DB40F7E TATA box-binding protein-associated The sequence BAD differs from that shown.
Probable cloning artifact. Full view. These are stable identifiers and should be used to cite UniProtKB entries. Do not show this banner again. Transcription , Transcription regulation.
Reactome - a knowledgebase of biological pathways and processes More Reactome i. It lists the nodes as they appear top-down in the taxonomic tree, with the more general grouping listed first. Human Gene Nomenclature Database More HGNC i. MIM i.
The interaction of Bacillus subtilis σA with RNA polymerase - Europe PMC Article - Europe PMC
DisGeNET i. Open Targets More OpenTargets i. PharmGKB i. BioMuta curated single-nucleotide variation and disease association database More BioMuta i. DMDM i. Phosphoserine Combined sources Manual assertion inferred from combination of experimental and computational evidence i Ref. Encyclopedia of Proteome Dynamics More EPD i.
TATA box-binding protein-associated factor RNA polymerase I subunit C
MassIVE i. MaxQB i. PaxDb, a database of protein abundance averages across all three domains of life More PaxDb i. PeptideAtlas More PeptideAtlas i.
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TAF1C - Function
ENSG Expressed in organ s , highest expression level in myometrium. ExpressionAtlas i. Q baseline and differential. Genevisible search portal to normalized and curated expression data from Genevestigator More Genevisible i. One study showed that the remaining wild type allele is required for leukemogenesis Thiel et al. The structural requirements of MLL fusion-dependent leukemic transformation can be evaluated using the ex vivo myeloid progenitor transformation assay Lavau et al. In this assay, a retrovirus carrying an MLL fusion gene is transduced into murine bone marrow-derived immature hematopoietic progenitors and the cells are cultured ex vivo in semi-solid media containing the required cytokines.
Transduction of a functional MLL fusion gene results in the cells expressing high Hoxa9 levels and continuing to proliferate after rounds of replating, while non-transduced cells stop proliferating during early passages Ayton and Cleary, The N-terminal region upstream of the AT hooks was shown to be required for transformation Figure 3A. Many epigenetic modifiers possess PWWP domains.
This H3K36me3 modification highlights transcribed regions and is required for efficient DNA damage response Mar et al. Therefore, heterozygous loss of SETD2, which leads to blunt DNA damage response against chemotherapy, is often found in relapsed leukemia Mullighan et al. SETD2 was recently reported to physically interact with MLL fusion proteins and may also be implicated in the efficient targeting of MLL fusion proteins to the target promoters Skucha et al. Unmethylated CpGs are an epigenetic mark of non-silenced promoters because methylation of CpGs in the promoter are associated with transcriptional silencing.
Therefore, it is likely that MLL targets CpG-rich promoters which were previously transcriptionally-active in the maternal cell and re-activates transcription in daughter cells to maintain the HOX gene expression patterns.
Resent research showed that the target chromatin of MLL fusion proteins is not confined to the promoter region. Localization of MLL fusion proteins spreads into the gene body at some MLL target genes, which are often hypo-methylated and highly transcribed Kerry et al. It has been suggested that this aberrant localization is implicated in disease progression. Moreover, in some genes MLL-ENL localizes near the transcription end site and activates gene expression predominantly at transcription elongation levels Garcia-Cuellar et al. These results suggest that MLL fusion proteins can be involved in multiple facets of gene activation through binding outside of the promoter region even though their primary targets are CpG-rich promoter regions.
While MLL fusion proteins target previously-active CpG-rich promoters through their MLL portions, the fusion partner portion confers the ability to activate transcription.
Therefore, functional modules retained within the AF4 portion were thought to be responsible for transformation. The minimum structure required for transformation was the region encompassing the SDE motif and the NKW motif, which recruit SL1 and activate transcription Okuda et al. These results suggest that the MLL fusion proteins transform myeloid progenitors via SL1-mediated transcriptional activation through AF4.
Taken together, these observations suggest that the major role of MLL fusion proteins in leukemic transformation is not to activate transcription elongation but to activate transcription initiation via SL1. Figure 4. Structural requirements of MLL fusion proteins for leukemic transformation. A Schematic representation of the structures of various MLL fusion constructs. Dotted lines indicate protein-protein interaction. Associated properties of each construct, such as the ability to immortalize myeloid progenitors, and the binding abilities to AF4, DOT1L, and ENL are shown on the right.
Immortalizing ability and AF4 binding ability through the TRX2 domain are highlighted in blue and red, respectively. One MISD, located at the residues —, was omitted because of its very weak affinity Kuntimaddi et al. Figure 5. Models of MLL fusion-dependent gene activation. AEP activates transcription via SL1.