Genomic profiling of a RYR1-deficient skeletal muscle

ABSTRACT: In differentiated skeletal muscle, intracellular Ca2+ concentrations rise dramatically upon membrane depolarization, constituting the link between excitation and contraction (EC). Transient rises in [Ca2+]i mainly emerge from Ca2+ released by the type 1 ryanodine receptor (RYR1) and, in non-adult muscle, by the inositol 1,4,5-triphosphate receptor (IP3R) of the sarcoplasmic reticulum (SR), the dominant Ca2+ store in skeletal muscle. While the IP3R-mediated, slow Ca2+ transients, have been implicated in cell signaling and development, RYR1’s non-contractile role(s) remain obscure. We used a homozygous mouse RyR1 knockout model (dyspedic) to investigate the effects of the absence of a functional RYR1 and, consequently, the lack of RyR1-mediated Ca2+ signaling during embryogenesis. While hete

INSTRUMENT(S): Maxwell 16 Instrument (Cat. #AS2000, Promega, Madison, WI), Affymetrix Gene-Chip Scanner-3000-7G, Genechip Hybridization Oven-645 (Affymetrix); Geneechip Fluidics Station-450 (Affymetrix)

ORGANISM(S): Mus musculus

SUBMITTER: Dilyana Filipova 

PROVIDER: E-MTAB-3608 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress