Ask about this productRelated genes to: LMOD3 antibody
- Gene:
- LMOD3 NIH gene
- Name:
- leiomodin 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2018-11-16
Related products to: LMOD3 antibody
Related articles to: LMOD3 antibody
- Xin'anjiang water buffalo (XAJB) is crucial for meat production and agricultural activities in Anhui Province of China. To generate hypotheses regarding how DNA methylation might correlate with transcriptional differences in skeletal muscle, WGBS and RNA-seq were performed on three BF and three BM adult XAJB. The results revealed 31,333 differentially methylated cytosines (DMCs), 1961 differentially methylated regions (DMRs), and 230 differentially expressed genes (DEGs) in skeletal muscle between the two groups. The qRT-PCR results of ten DEGs (, , , , , , , , and ) enriched in protein digestion and absorption pathway, PPAR signaling pathway, ECM-receptor interaction pathway or PI3K-Akt signaling pathway were consistent with the RNA-seq results. Most methylation changes occurred in CG context, and sixteen genes were predicted as dual differential genes in both methylation and transcriptome. Moreover, CG methylation showed a significant negative correlation with gene expression within the 2 kb upstream region (rho = -0.42, < 0.001). Given the limited number of animals examined, additional investigations with expanded cohorts are essential to verify the association between the methylome and transcriptome signatures underlying skeletal muscle in XAJB. - Source: PubMed
Publication date: 2026/02/10
Zhao ShuanpingJin HaiLiu JunLi YongshengLi QianZhang HuibinDu XinyiLi QinggangXu Lei - Genetic variation and lived experiences shape how our hearts respond to chronic stress and development of heart failure, manifested as compromised pumping function and abnormal hemodynamics. The hallmark of heart failure etiology is excessive stress signals followed by maladaptive structural, electrical, and functional changes to the heart muscle, also known as cardiac remodeling. The specific genetic mechanisms which underly such phenomenon, however, are still unclear, due in part to difficulties in accounting for environmental effects in human population studies. To overcome this challenge, we used the Collaborative Cross (CC) mouse population to investigate heritable susceptibility to cardiovascular stress through chronic β-adrenergic receptor stimulation with the β-agonist isoproterenol (ISO), which targets the common signaling gateway to heart failure, regardless of the particular upstream stressor. Across 8 founder and 63 CC lines, we measured nonfailing and failing heart characteristics represented by cardiac structure and function, organ weights, and cell morphology. Genome-wide QTL mapping detected 49 genome-wide significant loci, collapsing to 20 unique intervals (9 significant for multiple traits and 11 trait-specific), averaging 12.83 Mb in size. To identify high-confidence candidate genes from these loci, we augmented our trait mapping with coding variants drawn from sequencing data, tractability in an in vitro rat cardiomyocyte model, and previously reported protein functions and/or mouse or human phenotypes. This approach recovered both known regulators, such as Hey2, and new candidates. Functional tests in in vitro models highlight 3 candidate genes that modulate hypertrophic growth: Abcb10, Mrps5, and Lmod3. Abcb10 knockdown increased cell size at baseline and further with ISO, consistent with loss of a mitochondrial stress-buffering role. Mrps5 knockdown blunted stress-induced hypertrophy, possibly related to its previously known involvement in oxidative stress regulation. Lmod3 knockdown also attenuated hypertrophy, potentially via actin-assembly control under adrenergic stress. Together, these results reveal heritable pathways of β-adrenergic remodeling in mice and provide an interpretable, translational, and stepwise framework to prioritize candidate genes within broad loci for mechanistic studies of heart failure. - Source: PubMed
Kimball Todd HLuu Anh NGural BrianLahue CaitlinHockett AbigailRavindran SriramAli AmiraDalal AryanArdery SamSipko Emily LKirkland Logan GGoyal MansiJensen Brian CBerlow Rebecca BRau Christoph D - F-actin cytoskeleton plays critical roles in hair cell. This study identifies LMOD3, an F-actin nucleator, as specifically expressed in outer hair cells (OHCs) of mice. Lmod3 knockout causes significant hearing loss (about 40 dB elevation in auditory brainstem response (ABR) thresholds, increased distortion product otoacoustic emission (DPOAE) thresholds), while leaving stereocilia morphology and mechanoelectrical transduction (MET) function intact. Phenotypic analyses hint that LMOD3 deficiency likely impairs OHC-based cochlear amplification. Our work establishes LMOD3 as essential for auditory function. - Source: PubMed
Publication date: 2025/12/12
Du HaiboHuang XiSun YixiaoZhou Hao - Skeletal muscle is the largest tissue in mammals, and it plays a crucial role in metabolism and homeostasis. Skeletal muscle development and regeneration consist of a series of carefully regulated changes in gene expression. Leiomodin2 (LMOD2) gene is specifically expressed in the heart and skeletal muscle. But the physiological functions and mechanisms of LMOD2 on skeletal muscle development are unknown. - Source: PubMed
Publication date: 2025/07/31
Wang KaimingLiu CaihongYi LeiLiufu SuiChen WenwuLiu XiaolinChen BoheXu XinLiu JingwenLiu XibingYin YulongMa Haiming - Muscle contraction is a regulated process driven by the sliding of actin-thin filaments over myosin-thick filaments. Lmod2 is an actin filament length regulator and essential for life since human mutations and complete loss of Lmod2 in mice lead to dilated cardiomyopathy and death. To study the little-known role of Lmod2 in skeletal muscle, we created a mouse model with Lmod2 expressed exclusively in the heart but absent in skeletal muscle. Loss of Lmod2 in skeletal muscle results in decreased force production in fast- and slow-twitch muscles. Soleus muscle from rescued knockout mice have shorter thin filaments, increased Lmod3 levels, and present with a myosin fiber type switch from fast myosin heavy chain (MHC) IIA to the slower MHC I isoform. Since Lmod2 regulates thin-filament length in slow-twitch but not fast-twitch skeletal muscle and force deficits were observed in both muscle types, this work demonstrates that Lmod2 regulates skeletal muscle contraction, independent of its role in thin-filament length regulation. - Source: PubMed
Publication date: 2024/03/13
Larrinaga Tania MFarman Gerrie PMayfield Rachel MYuen MichaelaAhrens-Nicklas Rebecca CCooper Sandra TPappas Christopher TGregorio Carol C