anti-ADAM Metallopeptidase Domain 33 (ADAM33) Antibodies

Mouse (Murine) ADAM Metallopeptidase Domain 33 (ADAM33) interaction partners

1. Identification and preliminary characterization of mouse Adam33.

2. ADAM33 is not essential for growth or reproduction in the mouse and does not modulate baseline or allergen-induced airway responsiveness.

3. Adam33/Adam33 shows 2 significant increments in expression during lung morphogenesis, suggesting important developmental regulation.

Xenopus laevis ADAM Metallopeptidase Domain 33 (ADAM33) interaction partners

1. Here, the authors show that adam13 interacts with the arid3a/dril1 (show ARID3A Antibodies)/Bright transcription factor. This interaction promotes a proteolytic cleavage of arid3a (show ARID3A Antibodies) and its translocation to the nucleus where it regulates another transcription factor: tfap2alpha (show TFAP2A Antibodies). Tfap2alpha (show TFAP2A Antibodies) in turn activates multiple genes including the protocadherin pcdh8l (PCNS).

2. Increased ADAM13 cleavage of cadherin 11produces the EC1-3 fragment which increases cranial neural crest cell invasiveness in vitro and blocks the repulsive contact inhibition of locomotion response in colliding cells.

3. Novel roles for Plk and GSK3 regulation of ADAM13 function in cranial neural crest cell migration.

4. Data show that ADAM13 function is autonomous to cranial neural crest (CNC) tissue.

5. The cytoplasmic domain of ADAM13 regulates the expression of multiple genes in cranial neural crest, including the protease Calpain8-a.

Human ADAM Metallopeptidase Domain 33 (ADAM33) interaction partners

1. There was no significant difference in ADAM33 genotype and allele distributions between psoriasis and control groups (p > 0.05). CONCLUSIONS: ADAM33 V4 C/G rs2787094 polymorphism was not associated with psoriasis risk in the Turkish population.

2. A lower level of ADAM33 was also correlated with shorter overall survival and metastasis-free survival and was considered an independent prognostic factor suggesting that ADAM33 is a novel molecular biomarker of Triple-negative breast cancer and basal-like phenotype that might be useful as a prognostic factor.

3. IL4RA (show IL4R Antibodies) and ADAM33 variants may be risk markers of asthma exacerbations in type-2 inflammatory endotype. Precise endotyping may facilitate the identification of genetic risk markers of asthma exacerbations.

4. Collectively, our findings suggest that 1,25(OH)2D3 inhibits VEGF (show VEGFA Antibodies)-induced ASM (show SMPD1 Antibodies) cell proliferation by suppressing VEGFR2 (show KDR Antibodies) and ERK1/2 activation and downregulating ADAM33. Further studies of these mechanisms are needed to facilitate the development of treatments for smooth muscle hyperplasia-associated diseases of the airway such as asthma.

5. meta-analysis suggested that ADAM33 polymorphisms rs2280091, rs2280090, rs2787094, rs44707 and rs528557 were significantly associated with a high risk of childhood asthma

6. There was a significant difference in the frequency of ADAM33 V4 polymorphism in both, asthmatic and COPD (show ARCN1 Antibodies) patients groups. No significant differences were found for T1 polymorphism. However, there were significant differences when haplotypes and diplotypes of ADAM33 V4/T1 were compared in all three groups. It can be concluded that the polymorphism V4 of ADAM33 is associated with asthma or COPD (show ARCN1 Antibodies) in Venezuelan patients.

7. Evidence from this meta-analysis demonstrates that ADAM33 T1 polymorphism might be associated with increased susceptibility to asthma among Asian children and that ADAM33 F + 1, T2, S2, or V4 polymorphism may be unrelated to susceptibility of childhood asthma.

8. enhances ADAM-33 expression and airway smooth muscle cell proliferation

9. An association between ADAM33 gene polymorphism and impaired lung functions was detected in wood dust-exposed workers.

10. This meta-analysis demonstrates that the ADAM33 gene polymorphisms confer susceptibility to allergic rhinitis