Key result
Deletion of the TPM1 gene targeting αTM1 in mice resulted in embryonic lethality at E9.5 with enlarged, non-beating hearts and failure to assemble striated myofibrils.
αTM1 is required for sarcomere formation and stabilizing F-actin at cell-cell junctions during embryonic cardiac morphogenesis.
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αTM1 required for murine sarcomere assembly; leaves open its role in human congenital cardiac disease.
McKeown et al. (2014) studied Embryonic cardiac development. TPM1 gene deletion targeting αTM1 was evaluated on Cardiac morphogenesis, myofibril assembly, and adherens junction formation. Deletion of the TPM1 gene targeting αTM1 in mice resulted in embryonic lethality at E9.5 with enlarged, non-beating hearts and failure to assemble striated myofibrils.
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