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We present genetic and statistical evidence that the R320Q substitution in SMYD1 underlies an inherited form of the AnWj-negative blood group phenotype. The mechanism by which the mutation leads to this phenotype remains to be determined.
SMYD1 serves as an Serum Response Factor-interacting protein, enhances Serum Response Factor DNA binding activity, and is required for endothelial cell migration and tube formation to regulate angiogenesis.
SMYD1 and G6PD modulation are critical events for miR-206-mediated differentiation of rhabdomyosarcoma.
effects of gene mutations on ventricular development
HDGF functions as a transcriptional repressor of the SMYD1 gene through interaction with the transcriptional corepressor CtBP.
These findings provide functional evidence for a role of Smyd1, or any member of the Smyd family, in regulating cardiac energetics in the adult heart, which is mediated, at least in part, via modulating PGC-1alpha.
Smyd1 is responsible for restricting growth in the adult heart, with its absence leading to cellular hypertrophy, organ remodeling, and fulminate heart failure. Molecular studies reveal Smyd1 to be a muscle-specific regulator of gene expression and indicate that Smyd1 modulates expression of gene isoforms whose expression is associated with cardiac pathology. Activation of Smyd1 can prevent pathological cell growth.
This work illustrates a crucial role for SMYD1 in skeletal muscle physiology and myofibril integrity.
Deletion of Smyd1 impaired myoblast differentiation, resulted in fewer myofibers and decreased expression of muscle-specific genes
Smyd1 is required for maintaining cardiomyocyte proliferation at minimally two different embryonic heart developmental stages
suggest for the first time that, in addition to being a master redox regulator of protein disulfide bonds and nitrosation, Trx1 may also modulate lysine methylation, a non-redox post-translational modification, via the regulation of SMYD1 expression
the skNAC-Smyd1 complex is involved in transcriptional regulation both via the control of histone methylation and histone (de)acetylation.
skNAC binds to the E3 SUMO ligase mammalian Mms21/Nse2 and that knockdown of Nse2 expression inhibits specific aspects of myogenic differentiation, accompanied by a partial blockade of the nuclear-to-cytoplasmic translocation of the skNAC-Smyd1 complex
MYND domain may primarily serve as a protein interaction module and cooperate SmyD1 with skNAC to regulate cardiomyocyte growth and maturation.
The muscle-specific transcription factor skNAC is the major binding partner for Smyd1 in the developing heart.
Bop encodes a muscle-restricted protein containing MYND and SET domains and is essential for cardiac differentiation and morphogenesis.
Similar kinetics of induction and localization of m-Bop and skNAC during the induction of myogenesis in cultured C2C12 cells suggests a possible associated role for these proteins during this process.
BOP, a regulator of right ventricular heart development, is an essential downstream effector gene of MEF2C in the developing heart.
SmyD1a and SmyD1b are histone methyltransferases that play a critical role in myofibril organization during myofiber maturation.
Loss of zebrafish Smyd1a interferes with myofibrillar integrity without triggering the misfolded myosin response.
Acts as a transcriptional repressor. Essential for cardiomyocyte differentiation and cardiac morphogenesis.
CD8 beta opposite
, SET and MYND domain-containing protein 1
, histone-lysine N-methyltransferase SMYD1
, zinc finger, MYND domain containing 18
, CD8beta opposite strand
, histone-lysine N-methyltransferase Smyd1
, zinc finger protein BOP
, SET and MYND domain containing 1
, SET and MYND domain-containing 1
, SET and MYND domain containing protein
, SET and zf-MYND domain-containing protein
, SET and MYND domain-containing protein 1-like