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Data show that transcription factor activating enhancer binding protein-4 (TFAP4) is a direct transcriptional target of MYCN (show MYCN Proteins) in neuroblastoma (show ARHGEF16 Proteins) and that high levels of this transcription factor are associated with poor clinical outcome in this disease.
Depletion of either Arl5b (show ARL5B Proteins) or AP4 (show REPIN1 Proteins) results in the accumulation of APP (show APP Proteins).
results indicate that AP4 (show REPIN1 Proteins) is a central mediator and coordinator of cell cycle progression
the 16 SNP variants studied in the genes encoding the four units of AP-4 (show REPIN1 Proteins) do not have a major role in overall CP, but SNP rs1217401 of AP4B1 (show AP4B1 Proteins) is significantly associated with the risk of CP as a sequela of neonatal HIE in the Chinese population.
betaTrCP (show BTRC Proteins)-dependent degradation of TFAP4 is required for the fidelity of mitotic division
Senescence caused by AP4 (show REPIN1 Proteins)-deficiency was prevented by depletion of p16 and/or p21 (show CDKN1A Proteins), demonstrating that these factors mediate senescence caused by AP4 (show REPIN1 Proteins) loss.
Elevated AP4 (show REPIN1 Proteins) expression in primary colorectal cancer (CRC (show CALR Proteins)) significantly correlated with liver metastasis and poor patient survival. Findings imply AP4 (show REPIN1 Proteins) as a new regulator of epithelial-mesenchymal transition that contributes to metastatic processes in CRC (show CALR Proteins)
findings provide evidence that a high expression level of AP-4 (show REPIN1 Proteins) serves as a biomarker for poor prognosis for hepatocellular carcinoma
The expression of AP-4 (show REPIN1 Proteins) was silenced by the siRNAs transfection.
Overexpression of AP-4 (show REPIN1 Proteins) is associated with gastric carcinoma.
AP4 (show REPIN1 Proteins) integrates T-cell-mediated selection and sustained expansion of GC B (show NPR2 Proteins) cells for humoral immunity.
Induction of AP4 (show REPIN1 Proteins) by c-myc (show MYC Proteins) maintains CD8 (show CD8A Proteins)+ T cell activation.
Senescence caused by AP4 (show REPIN1 Proteins)-deficiency was prevented by depletion of p16 and/or p21, demonstrating that these factors mediate senescence caused by AP4 (show REPIN1 Proteins) loss.
AP4 (show REPIN1 Proteins) contributes to Cd4 (show CD4 Proteins) silencing both in DN and CD8 (show CD8A Proteins)(+) T cells by enforcing checkpoints for appropriate timing of CD4 (show CD4 Proteins) expression and its epigenetic silencing.
caspase-9 (show CASP9 Proteins) expression is regulated by the transcription factor activator protein-4 in glucocorticoid-induced apoptosis
Transcription factors of the basic helix-loop-helix-zipper (bHLH-ZIP) family contain a basic domain, which is used for DNA binding, and HLH and ZIP domains, which are used for oligomerization. Transcription factor AP4 activates both viral and cellular genes by binding to the symmetrical DNA sequence CAGCTG (Mermod et al., 1988
transcription factor AP-4 (activating enhancer binding protein 4)
, transcription factor AP-4
, transcription factor AP4
, activating enhancer-binding protein 4
, class C basic helix-loop-helix protein 41
, transcription factor AP-4 (activating enhancer-binding protein 4)