Anti-MyoD1 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

MyoD1 also known as Myogenic Differentiation 1 is a master regulator of muscle differentiation. It functions mechanically as a transcription factor binding to DNA at specific sequences thereby activating the transcription of genes necessary for muscle tissue development. MyoD1 has a molecular weight of approximately 45 kDa. It is expressed in skeletal muscle tissues and also detected in some non-muscle tissues though at lower levels. MyoD1 is essential in the early stages of muscle cell lineage commitment.

Biological function summary

MyoD1 plays an important role in muscle differentiation by activating muscle-specific genes. It belongs to the myogenic regulatory factor family and often operates within a protein complex alongside Myf5 and myogenin aiding in the conversion of mesodermal stem cells into muscle cells. These partnerships enhance its ability to initiate the muscle-specific gene expression that drives myogenesis. MyoD1 acts like a molecular switch shifting cells into the pathway leading to muscle formation.

Pathways

MyoD1 is an integral component of myogenesis and muscle regeneration pathways. MyoD1 interacts with key pathway components such as Myf5 and MRF4 which reinforce MyoD1 activity in muscle tissue lineage determination and cell cycle arrest during differentiation. The activity of MyoD1 in these pathways highlights its role in skeletal muscle growth. MyoD1 also demonstrates functional redundancy with Myogenin as both share overlapping roles in these critical pathways.

Associated diseases and disorders

MyoD1 is associated with muscular dystrophy and some sarcomas. Aberrant expression or mutations in MyoD1 can disrupt normal muscle differentiation contributing to muscle-related disorders like rhabdomyosarcoma a form of cancer comprising cells resembling skeletal muscle. Its relationship with other proteins like Myf5 further highlights its role in such pathological conditions as faults in these connections can amplify or alter disease progression.