Disease relevance of Myh9

• Localization of Myh9 within the stereocilia raises the possibility that mutations of MYH9 may effect hearing loss though disruption of the stereocilia structure [1].

High impact information on Myh9

• Here we show that nonmuscle myosin heavy chain IIA, or MyH9, is the only class II myosin expressed in T cells and is associated with the uropod during crawling [2].
• In contrast to NMHC II-A and II-B, the mRNA level in human fetal tissues is substantially lower than in adult tissues [3].
• The defects can be reproduced by introducing siRNA directed against NMHC II-A into wild-type embryonic stem cells [4].
• Here we show that mice ablated for NMHC II-A fail to develop a normal patterned embryo with a polarized visceral endoderm by E6.5 and die by E7 [4].
• These data indicate a role for CaM kinase stimulation and resultant threonine phosphorylation of NMHC-IIA in RBL-2H3 m1 cell activation [5].

Anatomical context of Myh9

• 5. The sensory cells of the developing cochlea were positive for Myh9 expression at E16 [6].
• Identification of Myh9 in the developing and mature inner ear suggests a role for this protein in the development and maintenance of auditory function [6].
• 5. Within the neonate and the adult cochlea, Myh9 expression was observed within the sensory hair cells and the supporting hair cells of the organ of Corti, the spiral ligament, and the spiral limbus, but not in the stria vascularis [6].
• 5. Myh9 expression was found to persist within the epithelia surrounding the cochlear duct at E13.5 and E16 [6].
• Myh9 is expressed predominantly within the spiral ligament as well as in the sensory hair cells of the organ of Corti [1].

Associations of Myh9 with chemical compounds

• Stimulation of RBL-2H3 m1 mast cells through the IgE receptor with antigen, or through a G protein-coupled receptor with carbachol, leads to the rapid appearance of phosphothreonine in nonmuscle myosin heavy chain II-A (NMHC-IIA) [5].

Other interactions of Myh9

• Cloning and developmental expression of nonmuscle myosin IIA (Myh9) in the mammalian inner ear [6].
• In contrast to most cells, cardiac myocytes lack NMHC II-A, and ablation of NMHC II-B results in a heart with 70% fewer myocytes at embryonic day 14.5 (E14.5) than control mice (B+/B- and B+/B+) [7].
• These data taken together strongly suggest that base-line expression of nonmuscle myosin IIA inhibits osteoclast precursor fusion and that a temporary, cathepsin B-mediated decrease in myosin IIA levels triggers precursor fusion during osteoclastogenesis [8].

Analytical, diagnostic and therapeutic context of Myh9

• Immunoblotting of embryonic (E15.5) and adult tissues from several organs, including the cochlea, identified a single 250-kDa anti-Myh9-immunoreactive band, supporting an absence of Myh9 splice variants in the fetus and the adult [6].
• Confocal microscopy of cochlear surface preparations, identified Myh9 within the inner and outer hair cells and their stereocilia [1].
• The phosphorylation site in rodent NMHC-IIA was localized to the carboxyl terminus of NMHC-IIA distal to the coiled-coil region, and identified as Thr-1940 by site-directed mutagenesis [5].

References