CLCKb mutation as a diagnostic therapeutical target

Details CLCKb mutation as a diagnostic therapeutical target CLCKb mutation as a diagnostic therapeutical target

2006-07-11

2006-07-11

Carlson, Karen Cochrane (Department: 1653)

Chemistry: molecular biology and microbiology

Measuring or testing process involving enzymes or...

Involving antigen-antibody binding, specific binding protein...

C530S350000

Reexamination Certificate

active

07074573

ABSTRACT:
The present invention relates to a method for diagnosing hypertension, and/or allergy, and/or hair loss, and/or liability for infection, of a human being, or a predisposition therefor; to a nucleic acid molecule coding for a human ClCKb protein comprising a genetic alteration at amino acid position481compared to the wild type, as well as for corresponding segments thereof; to a nucleic acid molecule which binds to the before-mentioned nucleic acid molecule under stringent conditions, as well as to a nucleic acid molecule which binds to that nucleic acid molecule; to a (poly)peptide encoded by the afore-mentioned nucleic acid molecules; to a method for identifying substances modulating activity of a peptide derived from ClCKb protein that is genetically altered at amino acid position481compared to the wild type; to a substance for modulating activity of a peptide derived from ClCKb protein that is genetically altered at amino acid position481compared to the wild type; to methods for preparing a pharmaceutical composition for treatment of hypertension, and/or allergy, and/or hair loss, and/or liability for infection; to pharmaceutical compositions; and to a method for treating a human being affected by hypertension, and/or allergy and/or hair loss, and/or liability for infection.

REFERENCES:
patent: WO 99/16909 (1999-01-01), None
patent: WO 01/73128 (2001-10-01), None
Waldegger et al. 2000; J. Am. Soc. Nephrol. 11: 1331-1339.
Jeck, N. et al. (2003) “Functional importance of CLCNKB genetics variants” Pediatric Nephrology, 18:13C, XP002314407.
Jeck, N. et al. (2003) “A common sequence variation of the CLCNKB gene strongly activates CLC-KB chloride channel activity (W22)”Nephrology Dialysis Transplantation Oxford 18:555, XP002314408.
Jeck, N. et al. (2004) “Activating mutation of the renal epithelial chloride channel CLC-KB predisposing to hypertension”Hypertension, 43:1175-1181.
Kieferle, S. et al. (1994) “Two highly homologous members of the CIC chloride channel family in both rat and human kidney”PNAS USA 91:6943-6947.
Konrad, M. et al. (2000) “Mutations in the chloride channel gene CLCNKB as a cause of classic barter syndrome”J. Am. Soc. Nephrol. 11:1449-1459.
Simon, D.B. et al. (1999) “Homo sapienschloride channel Kb (CLCNKB) mRNA”Database Genebank (1999) Online! NCBl: XP002314410.
Simon, D.B. et al. (1997) “Mutations in the chloride channel gene, CLCNKB, cause bartter' syndrome type III”Nature Genetics 17:171-178.
International Search report from co-pending application PCT/EP2004/011192.
Written Opnion from co-pending application PCT/EP2004/011192.

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