Disease relevance of Tcfap4

• During the isolation of apoptosis-related genes involved in glucocorticoid (GC)-induced cell death in murine thymic lymphomas, we found that the antisense gene of the transcription factor activator protein-4 (AP-4) inhibited dexamethasone-induced apoptosis [1].

High impact information on Tcfap4

• Here we report the isolation of the enhancer binding factor AP-4, which recognizes a motif in this domain [2].
• The deduced amino acid sequence reveals that AP-4 is a helix-loop-helix (HLH) protein [3].
• However, unlike other HLH proteins, AP-4 also contains two additional protein dimerization motifs consisting of leucine repeat elements LR1 and LR2 [3].
• Enhancer binding protein AP-4 is a transcription factor that activates both viral and cellular genes by binding to the symmetrical DNA sequence, CAGCTG [3].
• Like other members of this family, the AP-4 HLH motif and the adjacent basic domain are necessary and sufficient to confer site-specific DNA binding [3].

Chemical compound and disease context of Tcfap4

• When the cells were treated with dexamethasone, a rapid down-regulation of AP-4 and Casp-9 was observed whether the cells were GC-sensitive lymphomas or GC-insensitive L929 fibroblast cells [1].

Biological context of Tcfap4

• This sequence overlaps with the consensus sequences for transcription factors AP-1 and AP-4 [4].
• EMSA and Southwestern analysis revealed that defect in transcription activity in the NZB-derived segment is likely due to absence of transactivation by AP-4, which binds to the polymorphic 13 nucleotide deletion site [5].
• Functional binding of potential transcription factors to the octamer sequence, AP-4, and NFI sites was demonstrated by directed mutagenesis, electrophoretic mobility shift assay, and cross-linking [6].
• The AB1 fragment is composed largely of three tandem repeats containing two conserved core elements, A and B. Part of core element A (TCCGGAGCTGTG) resembles the consensus-binding site for transcription factor AP-4, whereas core element B (GCTGAGTCANGG) includes the consensus-binding site (TGAGTCA) for the AP-1 family of transcription factors [7].
• The 2 kb segment containing the immediate 5'-flanking and 5'-noncoding regions contain three consensus sequences for the NF-IL6 binding site, one consensus sequence for the NF-kappaB binding site, four AP-2 consensus sequences, one AP-4 consensus sequence, one potential cAMP response element, and one potential progesterone response element [8].

Anatomical context of Tcfap4

• The heterotetrameric adaptor protein (AP) complexes AP-1, AP-2, AP-3, and AP-4 play key roles in transport vesicle formation and cargo sorting in post-Golgi trafficking pathways [9].
• Electrophoretic mobility shift assays (EMSA) demonstrated that binding of AP-4- and AP-5-like proteins of mouse L and HeLa cells to the GT-II motif occurs in a mutually exclusive manner [10].

Associations of Tcfap4 with chemical compounds

• Immunofluorescence analyses showed that AP-4 is associated with the trans-Golgi network or an adjacent structure and that this association is sensitive to the drug brefeldin A [11].

Regulatory relationships of Tcfap4

• In contrast, both the expression and activation of Casp-9 were inhibited in the antisense AP-4 transfectants [1].

Other interactions of Tcfap4

• Western blot analysis revealed that the expression of Bcl-xL, Bax, and Apaf-1 was not affected in cells transfected with sense or antisense AP-4 genes [1].

Analytical, diagnostic and therapeutic context of Tcfap4

• Here, we report the molecular cloning and characterization of human AP-4 cDNAs [3].
• Chromatin immunoprecipitation experiments reveal that the interacting Igkappa gene cis-acting sequences are associated with AP-4, E47, and p65NF-kappaB, potential protein candidates that may be responsible for initiating and/or maintaining the formation of these higher-order complexes [12].
• Sequence analysis revealed several AP-1, AP-4, myo-D, GATA, and SP-1 sequences [13].

References