ArticleMolecular and cellular biology2003
Phenotypic analysis of Meltrin alpha (ADAM12)-deficient mice: involvement of Meltrin alpha in adipogenesis and myogenesis.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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Who cites it
52 citing papers in PubMed, 148 citations in OpenAlex.
- Functional ADAM12 variants modulate proteolytic activity and influence metabolic traits.Scientific reports · 2026Article
- Global A-to-I RNA editing during myogenic differentiation of goat MuSCs.Frontiers in veterinary science · 2024Article
- Large scale phenotype imputation and in vivo functional validation implicate ADAMTS14 as an adiposity gene.Nature communications · 2023Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- A Disintegrin and Metalloproteinase (ADAM) Family: Their Significance in Malignant Tumors of the Central Nervous System (CNS).International journal of molecular sciences · 2021Review
- ADAM12 is a costimulatory molecule that determines Th1 cell fate and mediates tissue inflammation.Cellular & molecular immunology · 2021Article
- Functions of 'A disintegrin and metalloproteases (ADAMs)' in the mammalian nervous system.Cellular and molecular life sciences : CMLS · 2019Review
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.Biochemical pharmacology · 2019Review
- Salt-Mediated Nanopore Detection of ADAM-17.ACS applied bio materials · 2019Article
- Knockdown of a disintegrin A metalloprotease 12 (ADAM12) during adipogenesis reduces cell numbers, delays differentiation, and increases lipid accumulation in 3T3-L1 cells.Molecular biology of the cell · 2018Article
- ADAM12 Is a Novel Regulator of Tumor Angiogenesis via STAT3 Signaling.Molecular cancer research : MCR · 2017Article
- A glucocorticoid- and diet-responsive pathway toggles adipocyte precursor cell activity in vivo.Science signaling · 2016Article
- Review
- ADAM12 and PAPP-A: Candidate regulators of trophoblast invasion and first trimester markers of healthy trophoblasts.Cell adhesion & migration · 2016Review
- ADAM12-directed ectodomain shedding of E-cadherin potentiates trophoblast fusion.Cell death and differentiation · 2015Article
- Targeting autocrine HB-EGF signaling with specific ADAM12 inhibition using recombinant ADAM12 prodomain.Scientific reports · 2015Article
- Evolution of Vertebrate Adam Genes; Duplication of Testicular Adams from Ancient Adam9/9-like Loci.PloS one · 2015Article
- Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15.Investigative ophthalmology & visual science · 2014Article
- Notch increases the shedding of HB-EGF by ADAM12 to potentiate invadopodia formation in hypoxia.The Journal of cell biology · 2013Article
- ADAM and ADAMTS family proteins and their role in the colorectal cancer etiopathogenesis.BMB reports · 2013Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Meltrin alpha (ADAM12) is a metalloprotease-disintegrin whose specific expression patterns during development suggest that it is involved in myogenesis and the development of other organs. To determine the roles Meltrin alpha plays in vivo, we generated Meltrin alpha-deficient mice by gene targeting. Although the number of homozygous embryos are close to the expected Mendelian ratio at embryonic days 17 to 18, ca. 30% of the null pups born die before weaning, mostly within 1 week of birth. The viable homozygous mutants appear normal and are fertile. Most of the muscles in the homozygous mutants appear normal, and regeneration in experimentally damaged skeletal muscle is unimpeded. In some Meltrin alpha-deficient pups, the interscapular brown adipose tissue is reduced, although the penetrance of this phenotype is low. Impaired formation of the neck and interscapular muscles is also seen in some homozygotes. These observations suggest Meltrin alpha may be involved in regulating adipogenesis and myogenesis through a linked developmental pathway. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a candidate substrate of Meltrin alpha, and we found that TPA (12-O-tetradecanoylphorbol-13-acetate)-induced ectodomain shedding of HB-EGF is markedly reduced in embryonic fibroblasts prepared from Meltrin alpha-deficient mice. We also report here the chromosomal locations of Meltrin alpha in the mouse and rat.
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