Ignet

Gene Information

Gene symbol: TFAP4

Gene name: transcription factor AP-4 (activating enhancer binding protein 4)

HGNC ID: 11745

Synonyms: AP-4, bHLHc41

Related Genes

#	Gene Symbol	Number of hits
1	CREB1	1 hits
2	FCGR2B	1 hits
3	IL2RA	1 hits
4	INS	1 hits
5	LEF1	1 hits
6	RUNX1	1 hits

Related Sentences

#	PMID	Sentence
1	12370366	Our data imply that because of the deficient AP-4 binding, the NZB-type Fcgr2b allele polymorphism results in up-regulation of IgG Ab responses through down-regulation of FcgammaRIIB1 expression levels in germinal center B cells, and that such polymorphism may possibly form the basis of autoimmune susceptibility in combination with other background contributing genes.
2	12672257	Insulin release was inhibited dose-dependently by both of the diadenosine polyphosphate analogues to the same degree as by Ap(4)A.
3	12672257	Ip(5)I and Ip(6)I antagonized Ap(5)A-mediated inhibition of insulin release. [(3)H]Thymidine incorporation into VSMC was not influenced by either synthetic diadenosine polyphosphate analogue, indicating that Ap(4)A does not act by itself in this case but (active) degradation products mediate the effect.
4	12672257	The data indicate the following. (1) Since nondegradable compounds inhibit insulin release as well as Ap(4)A, it is Ap(4)A itself and not any of its degradation products that induces this effect. (2) Diadenosine polyphosphate effects on cell proliferation are mediated via a degradation product in contrast to their effect on insulin release. (3) Ip(5)I and Ip(6)I act like antagonists.
5	12672257	Insulin release was inhibited dose-dependently by both of the diadenosine polyphosphate analogues to the same degree as by Ap(4)A.
6	12672257	Ip(5)I and Ip(6)I antagonized Ap(5)A-mediated inhibition of insulin release. [(3)H]Thymidine incorporation into VSMC was not influenced by either synthetic diadenosine polyphosphate analogue, indicating that Ap(4)A does not act by itself in this case but (active) degradation products mediate the effect.
7	12672257	The data indicate the following. (1) Since nondegradable compounds inhibit insulin release as well as Ap(4)A, it is Ap(4)A itself and not any of its degradation products that induces this effect. (2) Diadenosine polyphosphate effects on cell proliferation are mediated via a degradation product in contrast to their effect on insulin release. (3) Ip(5)I and Ip(6)I act like antagonists.
8	12672257	Insulin release was inhibited dose-dependently by both of the diadenosine polyphosphate analogues to the same degree as by Ap(4)A.
9	12672257	Ip(5)I and Ip(6)I antagonized Ap(5)A-mediated inhibition of insulin release. [(3)H]Thymidine incorporation into VSMC was not influenced by either synthetic diadenosine polyphosphate analogue, indicating that Ap(4)A does not act by itself in this case but (active) degradation products mediate the effect.
10	12672257	The data indicate the following. (1) Since nondegradable compounds inhibit insulin release as well as Ap(4)A, it is Ap(4)A itself and not any of its degradation products that induces this effect. (2) Diadenosine polyphosphate effects on cell proliferation are mediated via a degradation product in contrast to their effect on insulin release. (3) Ip(5)I and Ip(6)I act like antagonists.
11	15338474	Ap(4)A (diadenosine tetraphosphate) leads to an increase in blood glucose while it decreases insulin levels in plasma.
12	15338474	In conclusion Ap(4)A as a diabetogenetic compound is not likely to be responsible for the development of insulin resistance or of hyperlipidemia.
13	15338474	Ap(4)A seems to be involved in the development of diabetes mellitus by increasing blood glucose and decreasing plasma insulin as shown earlier, but not in diabetes mellitus-associated diseases such as insulin resistance or hyperlipidemia.
14	15338474	Ap(4)A (diadenosine tetraphosphate) leads to an increase in blood glucose while it decreases insulin levels in plasma.
15	15338474	In conclusion Ap(4)A as a diabetogenetic compound is not likely to be responsible for the development of insulin resistance or of hyperlipidemia.
16	15338474	Ap(4)A seems to be involved in the development of diabetes mellitus by increasing blood glucose and decreasing plasma insulin as shown earlier, but not in diabetes mellitus-associated diseases such as insulin resistance or hyperlipidemia.
17	15338474	Ap(4)A (diadenosine tetraphosphate) leads to an increase in blood glucose while it decreases insulin levels in plasma.
18	15338474	In conclusion Ap(4)A as a diabetogenetic compound is not likely to be responsible for the development of insulin resistance or of hyperlipidemia.
19	15338474	Ap(4)A seems to be involved in the development of diabetes mellitus by increasing blood glucose and decreasing plasma insulin as shown earlier, but not in diabetes mellitus-associated diseases such as insulin resistance or hyperlipidemia.
20	23028375	Here we apply PWAS ("proteome-wide analysis of SNPs"), a methodology based on quantitative mass spectrometry that enables rapid screening of SNPs for differential transcription factor binding, to 12 SNPs that are highly associated with type 1 diabetes at the IL2RA locus, encoding the interleukin-2 receptor CD25.
21	23028375	We report differential, allele-specific binding of the transcription factors RUNX1, LEF1, CREB, and TFAP4 to IL2RA SNPs rs12722508A, rs12722522C, rs41295061A, and rs2104286A and demonstrate the functional influence of RUNX1 at rs12722508 by reporter gene assay.