ArticleMolecular and cellular biology1993
An alternatively spliced mRNA from the AP-2 gene encodes a negative regulator of transcriptional activation by AP-2.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 123 citations in OpenAlex.
- Article
- Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates.Cells · 2020Review
- A Heterozygous Novel Mutation inFrontiers in pediatrics · 2020Article
- Calcium efflux activity of plasma membrane Ca2+ ATPase-4 (PMCA4) mediates cell cycle progression in vascular smooth muscle cells.The Journal of biological chemistry · 2014Article
- Transcriptional control of melanoma metastasis: the importance of the tumor microenvironment.Seminars in cancer biology · 2011Review
- Reduced TFAP2A function causes variable optic fissure closure and retinal defects and sensitizes eye development to mutations in other morphogenetic regulators.Human genetics · 2009Article
- Article
- Ku proteins interact with activator protein-2 transcription factors and contribute to ERBB2 overexpression in breast cancer cell lines.Breast cancer research : BCR · 2009Article
- Dominant-negative GCMB mutations cause an autosomal dominant form of hypoparathyroidism.The Journal of clinical endocrinology and metabolism · 2008Article
- Suppression of invasion and peritoneal carcinomatosis of ovarian cancer cells by overexpression of AP-2alpha.Oncogene · 2004Article
- Different mechanisms are implicated in ERBB2 gene overexpression in breast and in other cancers.British journal of cancer · 2003Article
- Review
- Transcription factor AP-2alpha is preferentially cleaved by caspase 6 and degraded by proteasome during tumor necrosis factor alpha-induced apoptosis in breast cancer cells.Molecular and cellular biology · 2001Article
- Expression of transcription factor AP-2 in colorectal adenomas and adenocarcinomas; comparison of immunohistochemistry and in situ hybridisation.Journal of clinical pathology · 2001Article
- Dominant-negative transcription factor AP-2 augments SB-2 melanoma tumor growth in vivo.Oncogene · 2001Article
- The retinoblastoma-related Rb2/p130 gene is an effector downstream of AP-2 during neural differentiation.Oncogene · 2001Article
- Failure in post-transcriptional processing is a possible inactivation mechanism of AP-2alpha in cutaneous melanoma.British journal of cancer · 2000Article
- AP-2 family members regulate basal and cAMP-induced expression of human chorionic gonadotropin.Nucleic acids research · 2000Article
- Activation of somatostatin receptor II expression by transcription factors MIBP1 and SEF-2 in the murine brain.Molecular and cellular biology · 1999Article
- Coactivator PC4 mediates AP-2 transcriptional activity and suppresses ras-induced transformation dependent on AP-2 transcriptional interference.Molecular and cellular biology · 1999Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
AP-2 is a retinoic acid-inducible and developmentally regulated activator of transcription. We have cloned an alternative AP-2 transcript (AP-2B) from the human teratocarcinoma cell line PA-1, which encodes a protein differing in the C terminus from the previously isolated AP-2 protein (AP-2A). This protein contains the activation domain of AP-2 and part of the DNA binding domain but lacks the dimerization domain which is necessary for DNA binding. Analysis of overlapping genomic clones spanning the entire AP-2 gene proves that AP-2A and AP-2B transcripts are alternatively spliced from the same gene. Both transient and stable transfection experiments show that AP-2B inhibits AP-2 transactivator function, as measured by an AP-2-responsive chloramphenicol acetyltransferase reporter plasmid. Furthermore, constitutive AP-2B expression in PA-1 cells causes a retinoic acid-resistant phenotype, anchorage-independent growth in soft agar, and tumorigenicity in nude mice, in a fashion similar to transformation of these cells by oncogenes. To determine the mechanism by which AP-2B exerts its inhibitory function, we purified bacterially expressed AP-2A and AP-2B proteins. While bacterial AP-2B does not bind an AP-2 consensus site, it strongly inhibits binding of the endogenous AP-2 present in PA-1 cell nuclear extracts. However, DNA sequence-specific binding of bacterially expressed AP-2A cannot be inhibited by bacterially expressed AP-2B. Therefore, inhibition of AP-2 activity by the protein AP-2B may require an additional factor or modification supplied by nuclear extracts.
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