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Clca1  -  chloride channel calcium activated 1

Mus musculus

Synonyms: Calcium-activated chloride channel family member 3, Calcium-activated chloride channel regulator 1, Clca2, Clca3, Gob5, ...
 
 
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Disease relevance of Clca3

 

High impact information on Clca3

  • We identified a gene called gob-5 that had a selective expression pattern in the airway epithelium with AHR [4].
  • Here, we show that gob-5, a member of the calcium-activated chloride channel family, is a key molecule in the induction of murine asthma [4].
  • Intratracheal administration of adenovirus-expressing antisense gob-5 RNA into AHR-model mice efficiently suppressed the asthma phenotype, including AHR and mucus overproduction [4].
  • The histopathologic observations were verified using quantitative gene expression analyses examining gob5 gene expression [5].
  • The goblet cell hyper/metaplasia and the expression of mucus-associated gene, gob5, were correspondingly reduced in the CCR1(-/-) mice [6].
 

Biological context of Clca3

  • In addition, the Western blot analysis of gob5 protein indicated that CCR1(-/-) mice have virtually no up-regulation of the protein at day 6 of infection compared with wild-type-infected mice [6].
 

Anatomical context of Clca3

 

Associations of Clca3 with chemical compounds

  • Our studies identified Clca3 as a novel downregulated gene of PGR that is a direct target of E2 regulation [8].
  • The calcium chloride-activated channel gene hCLCA1 (gob-5 in the mouse) has been suggested to increase MUC-5AC gene expression, and both are increased in asthmatic patients and murine models [9].
 

Other interactions of Clca3

  • The most highly induced gene at all time points was mclca3 (gob5), a putative calcium-activated chloride channel involved in the regulation of mucus production and/or secretion [10].
  • In addition, there was decreased mucus in the bronchoalveolar lavage fluid, decreased periodic-acid Schiff staining, and significantly less mucus-associated gob-5 mRNA and protein in anti-CXCR2-treated mice [11].
  • We hypothesized that this increased mucus was associated with mucosal expression of Muc5ac, a mucus gene expression in airways, and gob-5, a member of the Ca(2)(+)-activated chloride channel family [2].
  • OBJECTIVE: We sought to determine whether TNF-alpha increases gene expression of gob-5 and MUC-5AC and induces mucus cell metaplasia in vivo [9].
 

Analytical, diagnostic and therapeutic context of Clca3

  • In the present study, we performed real-time RT-PCR and in situ hybridization to investigate the regulation of Clca3 by P4 and determine the pattern of expression of Clca3 in the uterus during early pregnancy [8].
  • Airway gene products for gob-5 and MUC-5AC were determined by means of real-time PCR [9].

References

  1. Differential immune responses and pulmonary pathophysiology are induced by two different strains of respiratory syncytial virus. Lukacs, N.W., Moore, M.L., Rudd, B.D., Berlin, A.A., Collins, R.D., Olson, S.J., Ho, S.B., Peebles, R.S. Am. J. Pathol. (2006) [Pubmed]
  2. Respiratory syncytial virus in allergic lung inflammation increases Muc5ac and gob-5. Hashimoto, K., Graham, B.S., Ho, S.B., Adler, K.B., Collins, R.D., Olson, S.J., Zhou, W., Suzutani, T., Jones, P.W., Goleniewska, K., O'Neal, J.F., Peebles, R.S. Am. J. Respir. Crit. Care Med. (2004) [Pubmed]
  3. Inhibition of stem cell factor reduces pulmonary cytokine levels during allergic airway responses. Berlin, A.A., Lincoln, P., Tomkinson, A., Lukacs, N.W. Clin. Exp. Immunol. (2004) [Pubmed]
  4. Role of gob-5 in mucus overproduction and airway hyperresponsiveness in asthma. Nakanishi, A., Morita, S., Iwashita, H., Sagiya, Y., Ashida, Y., Shirafuji, H., Fujisawa, Y., Nishimura, O., Fujino, M. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  5. Deletion of TLR3 alters the pulmonary immune environment and mucus production during respiratory syncytial virus infection. Rudd, B.D., Smit, J.J., Flavell, R.A., Alexopoulou, L., Schaller, M.A., Gruber, A., Berlin, A.A., Lukacs, N.W. J. Immunol. (2006) [Pubmed]
  6. Deletion of CCR1 attenuates pathophysiologic responses during respiratory syncytial virus infection. Miller, A.L., Gerard, C., Schaller, M., Gruber, A.D., Humbles, A.A., Lukacs, N.W. J. Immunol. (2006) [Pubmed]
  7. Cloning and identification of the gene gob-5, which is expressed in intestinal goblet cells in mice. Komiya, T., Tanigawa, Y., Hirohashi, S. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  8. Steroid hormone regulation of Clca3 expression in the murine uterus. Jeong, J.W., Lee, K.Y., Lydon, J.P., DeMayo, F.J. J. Endocrinol. (2006) [Pubmed]
  9. Chronic exposure to TNF-alpha increases airway mucus gene expression in vivo. Busse, P.J., Zhang, T.F., Srivastava, K., Lin, B.P., Schofield, B., Sealfon, S.C., Li, X.M. J. Allergy Clin. Immunol. (2005) [Pubmed]
  10. Gene expression profiles reveal increased mClca3 (Gob5) expression and mucin production in a murine model of asbestos-induced fibrogenesis. Sabo-Attwood, T., Ramos-Nino, M., Bond, J., Butnor, K.J., Heintz, N., Gruber, A.D., Steele, C., Taatjes, D.J., Vacek, P., Mossman, B.T. Am. J. Pathol. (2005) [Pubmed]
  11. CXCR2 regulates respiratory syncytial virus-induced airway hyperreactivity and mucus overproduction. Miller, A.L., Strieter, R.M., Gruber, A.D., Ho, S.B., Lukacs, N.W. J. Immunol. (2003) [Pubmed]
 
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