Mmp20
- Known as:
- Mmp20
- Catalog number:
- 050912A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Mmp20
Related genes to: Mmp20
- Gene:
- MMP20 NIH gene
- Name:
- matrix metallopeptidase 20
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-23
- Date modifiied:
- 2014-11-19
Related products to: Mmp20
Related articles to: Mmp20
- Early childhood caries (ECC) results from a complex interplay of genetic and environmental factors. Polymorphisms of enamel formation genes may alter the susceptibility to ECC. - Source: PubMed
Publication date: 2026/04/30
Sharma ArunaMuthu M SVenkatesan VettriselviNuvvula SivakumarTiruvengadam Gayathri - Endometriosis is a heterogeneous, estrogen-dependent inflammatory disorder that affects up to 15% of reproductive age women. Progestin-based therapies are the most commonly prescribed initial treatment; however, approximately one-third of patients exhibit progestin resistance, leading to inadequate symptom relief and discontinuation. Given the role of epigenetic dysregulation in endometriosis and its impact on hormonal responsiveness, we aimed to identify if circulating leukocyte DNA methylation signatures were associated with progestin treatment response and could serve as a non-invasive predictive biomarker. - Source: PubMed
Publication date: 2026/03/18
Cevik E CansuMamillapalli RamanaiahSferruzza GiacomoMamillapalli PadmavathiTaylor Hugh S - To investigate the effects of commonly prescribed antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs) during early life on enamel development through a systematic review with quantitative synthesis. - Source: PubMed
Publication date: 2026/03/12
Zamri NadiaNgo HienCourt ElizabethSamaranayake LakshmanFakhruddin Kausar SadiaAmaechi Bennett TochukwuKhani Saniya - Matrix metalloproteinase (MMP) expression and function are highly context dependent, varying across physiological and pathological conditions. We previously documented the expression profiles of select MMPs in the ischemic brains of young male rodents. However, aging is a major risk factor for stroke in humans and is associated with vasculature alterations, increased oxidative stress, and elevated inflammation. In addition, sex differences have been reported in stroke incidence and severity. Despite this, the effects of age, sex, and species on brain MMP gene expression after cerebral ischemia/reperfusion (I/R) has not been systematically examined. Therefore, we investigated how age, sex, and species influence the mRNA expression of all known MMPs (22 total) in the brain following cerebral I/R. Moderate-to-severe neurological deficits were induced by transient middle cerebral artery occlusion (MCAO) followed by reperfusion in young and aged male and female C57BL/6 mice and in young male Sprague-Dawley rats. Brain tissue from the ipsilateral (ischemic) hemisphere was collected on post-MCAO day 1, and MMP mRNA levels were quantified by real-time PCR and expressed as fold change relative to the sham control group. Across species, MMP-3, MMP-8, MMP-12, MMP-13, MMP-19, MMP-20, and MMP-27 were upregulated in both rats and mice. Species-specific increases were also observed: MMP-1, MMP-7, MMP-9, MMP-14, MMP-21, and MMP-25 were upregulated only in rats, whereas MMP-10 was upregulated only in mice. The most strongly upregulated MMPs were MMP-12 in rats and MMP-3, MMP-10, and MMP-12 in mice. By contrast, MMP-15 and MMP-17 were downregulated in both species, whereas MMP-23 and MMP-24 were downregulated only in rats and mice, respectively. Within mice, MMP-3, MMP-10, MMP-12, MMP-19, MMP-20, and MMP-21 increased in both sexes and age groups, except for MMP-19 in aged males and MMP-21 in young males. MMP-14 increased only in females (young and aged), whereas MMP-27 increased only in males (young and aged). Notably, MMP-3, MMP-10, and MMP-12 were the three most highly upregulated MMPs in both male and female mice regardless of age. Overall MMP mRNA expression levels were higher in aged male mice and lower in aged female mice relative to sex-matched young mice. Among all MMPs examined, MMP-12 showed the most marked upregulation across species and, within mice, across age groups and sexes. Collectively, these findings demonstrate that brain MMP gene expression after cerebral I/R is modulated by age, sex, and species, underscoring the importance of incorporating these biological variables when targeting MMPs individually or in combination in preclinical rodent stroke models. - Source: PubMed
Publication date: 2026/02/26
Challa Siva ReddyBaker Isidra MVinayagam VisheshJackson Samantha NKhan NabeehaMada Sahil ReddyUnnam PavaniFornal Casimir AKlopfenstein Jeffrey DVeeravalli Krishna Kumar - DLX3 is a homeobox transcription factor essential for multiple organogenesis processes. Mutations in DLX3 cause trichodentoosseous syndrome (TDO), characterized by curly hair, sclerotic bone, enamel, and dentin defects as well as taurodontism. Phenotypic variability in TDO has been well documented, but its pathogenesis remains poorly understood. Here, we characterized three TDO families with distinct clinical features and identified a known DLX3 deletion (c.561_562del) and the first pathogenic splice-site variant (c.516+1_516+2insA). The proband with the splice-site mutation displayed a mesenchymal-dominant phenotype with severe dentin hypoplasia, enlarged pulp chambers, and hypertaurodontism but nearly normal enamel, whereas the mother and sister showed epithelial-dominant anomalies, including enamel hypoplasia and kinky hair. Minigene analysis demonstrated that c.516+1_516+2insA generated two aberrant transcripts encoding p.Val173Aspfs*28 and p.Arg120_Val173del. These mutant proteins localized mainly in the cytoplasm and showed markedly reduced transactivation activity. In cultured human dental pulp cells, DLX3 overexpression upregulated the odontoblastic markers DSPP, MMP20, and WNT10A. Chromatin immunoprecipitation and reporter assays further revealed that DLX3 directly activates WNT10A via a conserved enhancer (chr2:218,878,973_218,879,302) and three upstream binding sites. These findings expand the TDO mutational spectrum and suggest that differential mutant DLX3 expression may contribute to phenotypic variability, whereas disrupted regulation of WNT10A underlies dentin defects and taurodontism. - Source: PubMed
Wang Yin-LinLin Hua-ChiehChen Jung-TsuChang Hsiao-HuaHsieh Ting-FengHung Hsin-YaWang Shih-Kai