| The histone methyltransferase SMYD1 is induced by thermogenic stimuli in adipose tissue. | The histone methyltransferase SMYD1 is induced by thermogenic stimuli in adipose tissue.
Cicatiello AG, Nappi A, Franchini F, Nettore IC, Raia M, Rocca C, Angelone T, Dentice M, Ungaro P, Macchia PE. | 03/11/2024 |
| Resistance training up-regulates Smyd1 expression and inhibits oxidative stress and endoplasmic reticulum stress in the heart of middle-aged mice. | Resistance training up-regulates Smyd1 expression and inhibits oxidative stress and endoplasmic reticulum stress in the heart of middle-aged mice.
Tang J, Wu C, Xu Y, Yang B, Xi Y, Cai M, Tian Z. | 01/3/2024 |
| Musashi-2 causes cardiac hypertrophy and heart failure by inducing mitochondrial dysfunction through destabilizing Cluh and Smyd1 mRNA. | Musashi-2 causes cardiac hypertrophy and heart failure by inducing mitochondrial dysfunction through destabilizing Cluh and Smyd1 mRNA.
Singh S, Gaur A, Sharma RK, Kumari R, Prakash S, Kumari S, Chaudhary AD, Prasun P, Pant P, Hunkler H, Thum T, Jagavelu K, Bharati P, Hanif K, Chitkara P, Kumar S, Mitra K, Gupta SK. | 11/8/2023 |
| SMYD1a protects the heart from ischemic injury by regulating OPA1-mediated cristae remodeling and supercomplex formation. | SMYD1a protects the heart from ischemic injury by regulating OPA1-mediated cristae remodeling and supercomplex formation.
Szulik MW, Valdez S, Walsh M, Davis K, Bia R, Horiuchi E, O'Very S, Laxman AK, Sandaklie-Nicolova L, Eberhardt DR, Durrant JR, Sheikh H, Hickenlooper S, Creed M, Brady C, Miller M, Wang L, Garcia-Llana J, Tracy C, Drakos SG, Funai K, Chaudhuri D, Boudina S, Franklin S., Free PMC Article | 05/25/2023 |
| Perm1 regulates cardiac energetics as a downstream target of the histone methyltransferase Smyd1. | Perm1 regulates cardiac energetics as a downstream target of the histone methyltransferase Smyd1.
Oka SI, Sabry AD, Horiuchi AK, Cawley KM, O'Very SA, Zaitsev MA, Shankar TS, Byun J, Mukai R, Xu X, Torres NS, Kumar A, Yazawa M, Ling J, Taleb I, Saijoh Y, Drakos SG, Sadoshima J, Warren JS., Free PMC Article | 09/19/2020 |
| The data suggest that skNAC and Smyd1 might be major players in the processes of myofibrillogenesis and sarcomerogenesis, probably specifically at later stages. | siRNA-mediated inhibition of skNAC and Smyd1 expression disrupts myofibril organization: Immunofluorescence and electron microscopy study in C2C12 cells.
Berkholz J, Eberle R, Boller K, Munz B. | 04/6/2019 |
| 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. | Histone methyltransferase Smyd1 regulates mitochondrial energetics in the heart.
Warren JS, Tracy CM, Miller MR, Makaju A, Szulik MW, Oka SI, Yuzyuk TN, Cox JE, Kumar A, Lozier BK, Wang L, Llana JG, Sabry AD, Cawley KM, Barton DW, Han YH, Boudina S, Fiehn O, Tucker HO, Zaitsev AV, Franklin S., Free PMC Article | 10/6/2018 |
| 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. | The chromatin-binding protein Smyd1 restricts adult mammalian heart growth.
Franklin S, Kimball T, Rasmussen TL, Rosa-Garrido M, Chen H, Tran T, Miller MR, Gray R, Jiang S, Ren S, Wang Y, Tucker HO, Vondriska TM., Free PMC Article | 07/1/2017 |
| This work illustrates a crucial role for SMYD1 in skeletal muscle physiology and myofibril integrity. | Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray.
Stewart MD, Lopez S, Nagandla H, Soibam B, Benham A, Nguyen J, Valenzuela N, Wu HJ, Burns AR, Rasmussen TL, Tucker HO, Schwartz RJ., Free PMC Article | 12/17/2016 |
| Deletion of Smyd1 impaired myoblast differentiation, resulted in fewer myofibers and decreased expression of muscle-specific genes | Defective myogenesis in the absence of the muscle-specific lysine methyltransferase SMYD1.
Nagandla H, Lopez S, Yu W, Rasmussen TL, Tucker HO, Schwartz RJ, Stewart MD. | 06/28/2016 |
| Smyd1 is required for maintaining cardiomyocyte proliferation at minimally two different embryonic heart developmental stages | Smyd1 facilitates heart development by antagonizing oxidative and ER stress responses.
Rasmussen TL, Ma Y, Park CY, Harriss J, Pierce SA, Dekker JD, Valenzuela N, Srivastava D, Schwartz RJ, Stewart MD, Tucker HO., Free PMC Article | 02/27/2016 |
| 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 | Master redox regulator Trx1 upregulates SMYD1 & modulates lysine methylation.
Liu T, Wu C, Jain MR, Nagarajan N, Yan L, Dai H, Cui C, Baykal A, Pan S, Ago T, Sadoshima J, Li H., Free PMC Article | 01/16/2016 |
| the skNAC-Smyd1 complex is involved in transcriptional regulation both via the control of histone methylation and histone (de)acetylation. | skNAC and Smyd1 in transcriptional control.
Berkholz J, Orgeur M, Stricker S, Munz B. | 10/31/2015 |
| 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 | The E3 SUMO ligase Nse2 regulates sumoylation and nuclear-to-cytoplasmic translocation of skNAC-Smyd1 in myogenesis.
Berkholz J, Michalick L, Munz B. | 08/15/2015 |
| MYND domain may primarily serve as a protein interaction module and cooperate SmyD1 with skNAC to regulate cardiomyocyte growth and maturation. | Crystal structure of cardiac-specific histone methyltransferase SmyD1 reveals unusual active site architecture.
Sirinupong N, Brunzelle J, Ye J, Pirzada A, Nico L, Yang Z., Free PMC Article | 01/29/2011 |
| The muscle-specific transcription factor skNAC is the major binding partner for Smyd1 in the developing heart. | skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration.
Park CY, Pierce SA, von Drehle M, Ivey KN, Morgan JA, Blau HM, Srivastava D., Free PMC Article | 01/8/2011 |
| HDGF functions as a transcriptional repressor of the SMYD1 gene through interaction with the transcriptional corepressor CtBP. | Hepatoma-derived growth factor represses SET and MYND domain containing 1 gene expression through interaction with C-terminal binding protein.
Yang J, Everett AD., Free PMC Article | 01/21/2010 |
| 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. | m-Bop, a repressor protein essential for cardiogenesis, interacts with skNAC, a heart- and muscle-specific transcription factor.
Sims RJ 3rd, Weihe EK, Zhu L, O'Malley S, Harriss JV, Gottlieb PD. | 01/21/2010 |
| Bop encodes a muscle-restricted protein containing MYND and SET domains and is essential for cardiac differentiation and morphogenesis. | Bop encodes a muscle-restricted protein containing MYND and SET domains and is essential for cardiac differentiation and morphogenesis.
Gottlieb PD, Pierce SA, Sims RJ, Yamagishi H, Weihe EK, Harriss JV, Maika SD, Kuziel WA, King HL, Olson EN, Nakagawa O, Srivastava D. | 01/21/2010 |
| BOP, a regulator of right ventricular heart development, is an essential downstream effector gene of MEF2C in the developing heart. | BOP, a regulator of right ventricular heart development, is a direct transcriptional target of MEF2C in the developing heart.
Phan D, Rasmussen TL, Nakagawa O, McAnally J, Gottlieb PD, Tucker PW, Richardson JA, Bassel-Duby R, Olson EN. | 01/21/2010 |
| SmyD1a and SmyD1b are histone methyltransferases that play a critical role in myofibril organization during myofiber maturation. | SmyD1, a histone methyltransferase, is required for myofibril organization and muscle contraction in zebrafish embryos.
Tan X, Rotllant J, Li H, De Deyne P, Du SJ., Free PMC Article | 01/21/2010 |
| effects of gene mutations on ventricular development | Molecular mechanisms of ventricular hypoplasia.
Srivastava D, Gottlieb PD, Olson EN. | 01/21/2010 |