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Validated All-in-One™ qPCR Primer for MYOD1(NM_002478.5) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a nuclear protein that belongs to the basic helix-loop-helix family of transcription factors and the myogenic factors subfamily. It regulates muscle cell differentiation by inducing cell cycle arrest, a prerequisite for myogenic initiation. The protein is also involved in muscle regeneration. It activates its own transcription which may stabilize commitment to myogenesis. [provided by RefSeq].
Gene References into function
- The myogenic basic helix-loop-helix family of transcription factors, MyoD, Myf5, myogenin, and MRF4, can each activate the muscle differentiation program.
- MYOD1 hypermethylation plays an important role in colorectal cancer and may be a novel prognostic factor.
- MyoD modulates the rate of Id1 degradation and suggest a dynamic interplay of these factors
- Hypermethylation of MYOD1 is statistically significantly associated with poor disease outcome in cervical cancer.
- degradation is modulated by E12 and E47
- This review highlights studies of molecular mechanisms by which the muscle-specific myogenic basic helix-loop-helix protein MyoD interacts with other regulatory factors to coordinate gene expression in a controlled and ordered manner.
- The expression of MyoD1 was more sensitive but less specific in patients with rhabdomyosarcoma.
- Myogenin and myogenic differentiation factor D (MyoD) mRNAs increased (P < 0.05) in young and old, whereas myogenic factor (myf)-5 mRNA increased in young only (P < 0.05). Myf-6 protein increased (P < 0.05) in both young and old.
- The results establish that cdk9/cyclin T2a-mediated coactivation of MyoD depends on serine 37 phosphorylation.
- MyoD below a threshold level and its displacement from the mitotic chromatin could present another window in the cell cycle for resetting the myogenic transcriptional program and to maintain the myogenic determination of the proliferating cells.
- MYOD1 is a positive diagnostic for biliary tract rhabdomyosarcoma.
- Expression of both the endogenous MyoD gene and a reporter gene driven by MyoD regulatory elements is similar in wild-type and homozygous null Gig1(nlacZ) transgenic MyoD1 mouse embryos.
- identified a negative regulatory element in the alpha-SG distal promoter including two conserved E-boxes (E1 and E2), which interact with MyoD
- a nonconventional interaction between HP1 and a tissue-specific transcription factor, MyoD. In addition, they strongly suggest that HP1 isoforms play important roles during muscle terminal differentiation in an isoform-dependent manner.
- NFAT and MyoD cooperation regulates myogenin expression and myogenesis
