Ask about this productRelated genes to: C1orf51 antibody
- Gene:
- CIART NIH gene
- Name:
- circadian associated repressor of transcription
- Previous symbol:
- C1orf51
- Synonyms:
- BC017397
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-02
- Date modifiied:
- 2014-11-19
Related products to: C1orf51 antibody
Related articles to: C1orf51 antibody
- Osteoporosis is a prevalent disorder characterized by reduced bone mass and deterioration of bone microstructure, leading to an increased risk of fractures. The osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) plays a critical role in bone formation. Circular RNAs (circRNAs) have been implicated in various diseases, including osteoporosis, by modulating gene expression. This study explores the role of circCacna1c in osteogenic differentiation and its potential as a therapeutic target for osteoporosis. CircCacna1c expression was downregulated in OVX mice and upregulated during osteogenic differentiation of BMSCs. Overexpression of circCacna1c promoted osteogenesis by increasing key osteogenic markers, such as Runx2, Ocn, and Alp. CircCacna1c was found to act as a molecular sponge for miR-7669-3p, which targets Ciart, enhancing its expression. The miR-7669-3p/Ciart axis played a crucial role in osteogenic differentiation, with knockdown of Ciart reversing the osteogenic-promoting effects of circCacna1c. In conclusions, the circCacna1c/miR-7669-3p/Ciart pathway is involved in regulating the osteogenic differentiation of BMSCs and may serve as a potential therapeutic target for osteoporosis. Modulating circCacna1c expression or its downstream signaling could offer novel strategies for the treatment and management of osteoporosis. - Source: PubMed
Publication date: 2025/12/09
Chen ZhipengLi YanChen Bailing - Heart failure (HF) represents the end stage of cardiovascular disease and is the leading cause of mortality. The objective of this study was to identify potential biomarkers and elucidate the mechanisms underlying the development of HF across diverse populations and among different genders. - Source: PubMed
Publication date: 2025/10/14
Yu YueXue ChentianJi DongSheng WeiGao XiangWu XizeWu Chengyan - Cardiac fibrosis, marked by excessive extracellular matrix deposition, leads to heart failure. This study examines the effects of bovine milk exosomes on cardiac fibrosis in an isoproterenol-induced rat model. Rats were orally administered bovine milk exosomes, and transcriptome sequencing of the left ventricle was conducted. We identified 116 differentially expressed mRNAs (DEMs) and 141 differentially expressed lncRNAs (DELs). Key DEMs (Ciart, Cd151, Per2, Per3, H3f3c, Dbp, Tnc) and DELs (XR_001841620.1, TCONS_00025336, TCONS_00002367, TCONS_00027989, TCONS_00029872, TCONS_00036358) were significantly upregulated, as confirmed by RT-qPCR. Gene Ontology and KEGG analysis showed enrichment in circadian rhythms and immune activities. Co-expression and competing endogenous RNA networks illustrated potential regulatory mechanisms. These findings elucidate the therapeutic effects of bovine milk exosomes on cardiac fibrosis, highlighting potential targets for future clinical research. - Source: PubMed
Publication date: 2025/10/08
Hu JiajiaLu XiaoxuYan JianqinWang JianZhang JunjieZhu HongWang EZhang Chengliang - Cancer patients experience circadian rhythm disruptions during and after chemotherapy that can contribute to debilitating side effects. It is unknown how chemotherapy mediates circadian disruptions and specifically the extent to which these disruptions occur at the level of the principal clock, the suprachiasmatic nuclei (SCN) of the hypothalamus. In the present study, we assessed how the commonly used chemotherapeutic, paclitaxel, impacts the SCN molecular clock and SCN-dependent behavioral adaptations to circadian challenges in female mice. Following a repeated chemotherapy regimen, we measured rhythmic SCN expression of molecular clock and circadian-associated transcripts. Paclitaxel chemotherapy disrupted the SCN molecular clock through abolished rhythmicity (, ) and damped rhythmic transcription (, , , ) of key molecular clock genes. We further determined chemotherapy-induced changes to SCN function by measuring circadian wheel running adaptations to a jet lag phase-delay or phase-advance paradigm and by generating a phase response curve (PRC). Chemotherapy did not alter re-entrainment to a 6 h phase-advance, but after a 6 h phase-delay, chemotherapy-treated mice had a more stable and robust circadian rhythm than vehicle-treated mice, possibly indicative of a weakened or decoupled SCN. In the PRC, chemotherapy blunted light-induced phase-shift delays during subjective night compared with vehicle controls, also indicative of disrupted SCN-dependent entrainment. Together, this work demonstrates that paclitaxel chemotherapy disrupts both the molecular clock and functional re-entrainment of the SCN that could cause or contribute to observed circadian rhythm disruptions after treatment. This research could help guide application of circadian-mediated therapies to mitigate side effects of chemotherapy. - Source: PubMed
Publication date: 2025/09/22
Tapp Zoe MSeng Melina MGhosh Amiya KObrietan Karl HPyter Leah M - As a major contributor to the development of major depressive disorder (MDD) in adolescents, circadian rhythm disruption has been linked with aberrant circadian protein levels and suprachiasmatic nucleus (SCN) activity. However, it remains unclear how the function of SCN underlies the association between circadian rhythm disruption and depression among adolescents. - Source: PubMed
Publication date: 2025/08/06
Guo QianruQiao DanZhai PeiyunZhang RongWen YujiaoLiu PenghongLi GaizhiLiu Zhifen