Cochleosaccular degeneration of the inner ear and progressive cataracts

Also Known As:

Networked: 1 relevant articles (0 outcomes, 1 trials/studies)

Disease Context: Research Results

Related Diseases

1.	Hearing Loss (Hearing Impairment)
2.	MYH9-Related Disorders

Experts

1.	Castelein, C M: 1 article (11/2000)
2.	Goldstein, J A: 1 article (11/2000)
3.	Kelley, M J: 1 article (11/2000)
4.	Lalwani, A K: 1 article (11/2000)
5.	Luxford, W: 1 article (11/2000)
6.	Mhatre, A N: 1 article (11/2000)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Cochleosaccular degeneration of the inner ear and progressive cataracts:

1.	Myosin Type IIIBA 11/01/2000 - "Previous studies have shown that modification of amino acid residues within the SH1 helix causes dysfunction of the ATPase activity of the motor domain in myosin II. Both the precise role of MYH9 in the cochlea and the mechanism by which the R705H mutation leads to the DFNA17 phenotype (progressive hearing impairment and cochleosaccular degeneration) remain to be elucidated."
2.	Amino AcidsFDA Link 11/01/2000 - "Previous studies have shown that modification of amino acid residues within the SH1 helix causes dysfunction of the ATPase activity of the motor domain in myosin II. Both the precise role of MYH9 in the cochlea and the mechanism by which the R705H mutation leads to the DFNA17 phenotype (progressive hearing impairment and cochleosaccular degeneration) remain to be elucidated."
3.	Adenosine Triphosphatases (ATPase)IBA 11/01/2000 - "Previous studies have shown that modification of amino acid residues within the SH1 helix causes dysfunction of the ATPase activity of the motor domain in myosin II. Both the precise role of MYH9 in the cochlea and the mechanism by which the R705H mutation leads to the DFNA17 phenotype (progressive hearing impairment and cochleosaccular degeneration) remain to be elucidated."