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Validated All-in-One™ qPCR Primer for TCF4(NM_001083962.2) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes transcription factor 4, a basic helix-turn-helix transcription factor. The encoded protein recognizes an Ephrussi-box ('E-box') binding site ('CANNTG') - a motif first identified in immunoglobulin enhancers. This gene is expressed predominantly in pre-B-cells, although it is found in other tissues as well. Defects in this gene are a cause of Pitt-Hopkins syndrome. Multiple alternatively spliced transcript variants that encode different proteins have been described.
Gene References into function
- dHAND/E-protein (E2A, ME2, and ALF1) heterodimers have distinct DNA binding specificities
- Competitive RT-PCR-based promoter activity assay showed that over-expression of ITF2B protein inhibited the expression of IL-2Ralpha gene in Jurkat cells in an NRE-dependent manner
- haploinsufficiency of TCF4 causes PHS and suggest that D. rerio is a valuable model to study the molecular pathogenesis of Pitt-Hopkins syndrome and the role of TCF4 in brain development
- Interstitial deletion involving TCF4 is associated with severe developmental delay and multiple abnormalities.
- Protein sequence alignment of the closely related bHLH transcription factors ITF-2B, HeLa E box protein (HITF4), and the E2A proteins E12 and E47 revealed the presence of a highly conserved protein domain.
- Gene disruption of TCF4 is associated with mental retardation but not always associated with Pitt-Hopkins syndrome.
- based on results, it is proposed that the observed frequent epigenetic-mediated TCF4 silencing plays a role in tumor formation and progression
- findings suggest that the concurrent action of Spi-B and E2-2 controls the development of progenitor cells into the plasmacytoid dendritic cell lineage
- Snail and Slug promote formation of beta-catenin-T-cell factor (TCF)-4 transcription complexes that bind to the promoter of the TGF-beta3 gene to increase its transcription
- These results identify E2-2 as a specific transcriptional regulator of the plasmacytoid dendritic cells lineage in mice and humans and reveal a key function of E proteins in the innate immune system.
- BCL-W may function as a downstream effector of inappropriate WNT/beta-catenin signalling.