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ADAM metallopeptidase domain 33

ADAM33, a disintegrin and metalloprotease 33
This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. This protein is a type I transmembrane protein implicated in asthma and bronchial hyperresponsiveness. Alternative splicing of this gene results in two transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: metalloprotease, POLYMERASE, HAD, AGE, IgE
Papers on ADAM33
ADAM33 and ADAM12 genetic polymorphisms and their expression in Egyptian children with asthma.
Abdelaziz Almalky et al., Az Zaqāzīq, Egypt. In Ann Allergy Asthma Immunol, Jan 2016
OBJECTIVES: To assess the association between ADAM33 and ADAM12 single-nucleotide polymorphisms (SNPs) with asthma risk and severity and to investigate the effect of ADAM33 and ADAM12 polymorphisms on expression of these proteases in sputum.
Genetic variants of ADAM33 are associated with asthma susceptibility in the Punjabi population of Pakistan.
Bano et al., Lahore, Pakistan. In J Asthma, Jan 2016
OBJECTIVE: A disintegrin and metalloproteinase 33 (ADAM33) gene has been considered as an asthma susceptibility gene due to its possible role in airway remodeling, abnormal cell proliferation and differentiation.
Association between ADAM33 S2 and V4 polymorphisms and susceptibility to allergic rhinitis: A meta-analysis.
Ding et al., Xiaogan, China. In Allergol Immunopathol (madr), Dec 2015
BACKGROUND: It has been reported that ADAM33 (a disintegrin and metalloproteinase domain 33) polymorphisms might be associated with susceptibility to allergic rhinitis (AR).
Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers.
Mahdy-Abdallah et al., Al Jīzah, Egypt. In Hum Exp Toxicol, Nov 2015
UNASSIGNED: ADAM33 represents an important gene of susceptibility for lung function impairment.
The ADAM33 S2 polymorphism is associated with susceptibility to pediatric asthma in the Chinese Han population.
Zhao et al., Linyi, China. In Genet Test Mol Biomarkers, Oct 2015
BACKGROUND: The disintegrin and metalloprotease domain containing protein 33 (ADAM33) is a novel susceptibility gene for asthma and airway hyperresponsiveness, particularly in the Asian population.
Compartment-specific expression of collagens and their processing enzymes in intrapulmonary arteries of IPAH patients.
Kwapiszewska et al., Graz, Austria. In Am J Physiol Lung Cell Mol Physiol, Jun 2015
Localization of COLXVIII, its cleavage product endostatin, and MMP10, ADAM33, and TIMP1 was confirmed in pulmonary arteries by immunohistochemistry. ELISA for collagen XVIII/endostatin demonstrated significantly elevated plasma levels in IPAH patients compared with donors, whereas circulating MMP10, ADAM33, and TIMP1 levels were similar between the two groups.
A disintegrin and metalloprotease 33 polymorphism association with COPD in long-term tobacco smokers of the ethnic Kashmiri population of India.
Koul et al., Jammu, India. In Lung India, May 2015
The 'A disintegrin and metalloprotease 33' (ADAM 33) gene is one candidate gene that has been studied.
ADAM33 polymorphisms and susceptibility to allergic rhinitis: a meta-analysis.
Zhang et al., Wuhan, China. In Eur Arch Otorhinolaryngol, Mar 2015
Several polymorphisms in a disintegrin and metalloproteinase 33 (ADAM33) have been implicated in susceptibility to allergic rhinitis (AR), but the results are inconclusive.
ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.
Ludwig et al., Aachen, Germany. In Am J Physiol Lung Cell Mol Physiol, Mar 2015
ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development.
An ADAM33 polymorphism associates with progression of preschool wheeze into childhood asthma: a prospective case-control study with replication in a birth cohort study.
Dompeling et al., Maastricht, Netherlands. In Plos One, 2014
RESULTS: In the ADEM study, the minor alleles of ADAM33 rs511898 and rs528557 and the ORMDL3/GSDMB rs7216389 polymorphisms were negatively associated, whereas the minor alleles of IL4 rs2243250 and rs2070874 polymorphisms were positively associated with childhood asthma.
Polymorphisms in a disintegrin and metalloprotease 33 gene and the risk of chronic obstructive pulmonary disease: a meta-analysis.
Cheng et al., Chengdu, China. In Respirology, 2014
A number of polymorphisms in a disintegrin and metalloprotease 33 (ADAM33) gene have been implicated in susceptibility to chronic obstructive pulmonary disease (COPD).
ADAM metallopeptidase domain 33 (ADAM33): a promising target for asthma.
Gao et al., Baltimore, United States. In Mediators Inflamm, 2013
Over the last few years, a significant progress has been made in understanding the role of a disintegrin and metalloproteinase 33 (ADAM33) in asthma.
Mechanisms of asthma and implications for its prevention and treatment: a personal journey.
Holgate, Southampton, United Kingdom. In Allergy Asthma Immunol Res, 2013
Varied activation of the EMTU connects the origins of asthma to its progression over time with involvement of epithelial susceptibility through impaired barrier and innate immune functions and altered mesenchymal susceptibility as exemplified by polymorphisms of the metalloprotease gene, ADAM33.
T1 and T2 ADAM33 single nucleotide polymorphisms and the risk of childhood asthma in a Saudi Arabian population: a pilot study.
Al-Muhsen et al., Riyadh, Saudi Arabia. In Ann Saudi Med, 2012
ADAM33 polymorphisms, but not S1 or ST+4, were significantly associated with asthma development in Saudi children, like those reported for white and Hispanic populations in the United States
Regulation of a disintegrin and metalloprotease-33 expression by transforming growth factor-β.
Davies et al., Southampton, United Kingdom. In Am J Respir Cell Mol Biol, 2012
This may provide a mechanism for fine regulation of levels of ADAM33 expression in fibroblasts, and may self-limit TGF-beta(2)-induced ectodomain shedding of ADAM33.
[Association of the MMP3, MMP9, ADAM33 and TIMP3 genes polymorphic markers with development and progression of chronic obstructive pulmonary disease].
Victorova et al., In Mol Biol (mosk), 2012
The ADAM33 gene polymorphism may be an important risk factor for the development and progression of chronic obstructive pulmonary disease.
ADAM33 genetic polymorphisms, smoking, and rhinoconjunctivitis in Japanese women: the Kyushu Okinawa Maternal and Child Health Study.
Arakawa et al., Fukuoka, Japan. In Hum Immunol, 2012
Our results suggest that SNPs and haplotypes in the ADAM33 gene are associated with rhinoconjunctivitis.
ADAM33 as a psoriasis susceptibility gene in the Han population of northeastern China.
Li et al., Harbin, China. In Dermatology, 2010
ADAM33 polymorphisms are associated with psoriasis in the northeastern Chinese Han population. The rs512625AA rs612709AA GA genotypes and haplotype H8 may be protective against psoriasis.
ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23.
Blobel et al., New York City, United States. In Nat Immunol, 2006
Here we used loss-of-function and gain-of-function experiments with cells lacking or overexpressing candidate CD23-releasing enzymes (ADAM8, ADAM9, ADAM10, ADAM12, ADAM15, ADAM17, ADAM19 and ADAM33), ADAM-knockout mice and a selective inhibitor to identify ADAM10 as the main CD23-releasing enzyme in vivo.
Association of the ADAM33 gene with asthma and bronchial hyperresponsiveness.
Keith et al., Waltham, United States. In Nature, 2002
genome-wide scan on 460 Caucasian families identified a locus on chromosome 20p13 that was linked to asthma (log(10) of the likelihood ratio (LOD), 2.94) and bronchial hyperresponsiveness (LOD, 3.93)
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