C1orf102
- Known as:
- C1orf102
- Catalog number:
- 002813A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C1orf102
Related genes to: C1orf102
- Gene:
- OSCP1 NIH gene
- Name:
- organic solute carrier partner 1
- Previous symbol:
- C1orf102
- Synonyms:
- NOR1
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-15
- Date modifiied:
- 2019-02-26
Related products to: C1orf102
Related articles to: C1orf102
- The coordination of pollen maturation and anther dehiscence is essential for cereal fertility, yet the metabolic mechanisms linking these processes remain poorly understood. Here, we demonstrate that the rice cysteine protease PAI1 (Pollen Anther Integrator 1) functions as a quantitative metabolic coordinator during rice male reproduction. Unlike canonical cysteine protease mutants that exhibit complete male sterility due to blockage of programmed cell death (PCD), pai1 mutants display partial male sterility characterized by two distinct metabolic defects: approximately 50% pollen abortion and defective anther dehiscence, resulting in an approximately 75% reduction in seed set. PAI1 localizes to the endoplasmic reticulum (ER) and plasma membrane (PM), where its proteolytic activity generates free amino acid pools required for maintaining amino acid homeostasis. Integrated metabolomic and transcriptomic analyses revealed that PAI1 loss-of-function is associated with selective depletion of protein-derived and aromatic amino acids during the critical developmental transition (stages 10-11), which correlates with reduced phenylpropanoid flux for endothecium lignification and fatty acid metabolism for pollen wall formation, without blocking PCD execution. The transcriptional regulators TDR, bHLH142, and AIP1 directly activate PAI1 expression by binding to overlapping cis-regulatory elements. Relative expression analysis further showed that OsCP1 and other network components are upregulated in pai1 mutants, reflecting an incomplete compensatory response, while the residual approximately 25% fertility likely arises from partial functional redundancy within the broader PAI1-like gene family. Together, these findings support a working model in which PAI1-mediated proteolysis quantitatively coordinates amino acid flux toward specific anabolic pathways, revealing a distinct class of cysteine proteases that may regulate developmental metabolic transitions beyond their established role in PCD execution. - Source: PubMed
Publication date: 2026/08/28
Tian JingfeiHe JuanXu YiboBao JinlinWei JianxinZhao WenfengShen ZejunWei ZihanWu MinghangWang PengpengMo JunLuo JijingQin Baoxiang - Hypoxia is a hallmark of tumor microenvironments that promotes bladder cancer (BCa). We aimed to study the upstream transfector of ROC1 on malignant oncological characteristics of BCa cells under hypoxic conditions, and clarified the regulating mechanisms involved. The expressions of ROC1 and HIF1A were mediated by RT-qPCR and western blot. The upstream transcription factor of ROC1 was analyzed by bioinformatic analysis and examined by clinical data. The BCa cell lines (T24 and 5637) were treated CREB1 overexpression or knockdown. The hypoxia induction was conducted, and cell proliferation, apoptosis, migration and invasion were subsequently studied. The rescue experiments in vitro and in vivo were performed to explore the underlying regulating mechanism of CREB1. ROC1 was down-regulated in bladder cancer tissues and hypoxia condition. CREB1 was an upstream transcription factor of ROC1. CREB1 expression was correlated with T Stage in BCa, while ROC1expression was associated with N Stage in BCa patients. CREB1 promoted the proliferation and inhibited the apoptosis of BCa cells under hypoxia. CREB1 regulated the invasion, migration, and expressions of Bcl−2, Bax, cleaved caspased−3, MMP2, and MMP9 in BCa cells under hypoxia. Down-regulation of ROC1 reversed CREB1’s effect on BCa cells. Similarly, HIF1A knockdown also reversed CREB1’s impact on BCa cells. CREB1 promoted tumor growth in vivo and shROC1 reversed its effect. Our study indicated that CREB1-ROC1 axis is a hypoxia-responsive therapeutic target in BCa, which can provide new insights for BCa early screening, prevention and treatment. - Source: PubMed
Publication date: 2026/04/04
Sun ZhenchaoWang YingyuYou ShengjieJi QingfenLiu XiangBao PengfeiZhang HuijiangZhou XiaoqingYe JunjieLi PengWu Qi - To investigate the effect of sennoside A (SA) on atherosclerosis (AS) in type 2 diabetes mellitus (T2DM) mice and its underlying mechanisms. - Source: PubMed
Publication date: 2026/03/23
Liu Mei-ZhiMa LiMi MengJiang Ya-NingWang Zi-YangSun Yong-Ning - Methane (CH) emissions present a significant challenge to both environmental sustainability and energy efficiency in ruminants, including beef cattle that are born in dairy herds. Although numerous approaches, including alterations in feed and the use of additives, are under investigation to mitigate these emissions, the genetic selection of animals that produce lower levels of methane offers the potential for enduring and cumulative advantages. Transcriptome analysis represents a crucial advancement in elucidating the networks and mechanisms through which the ruminant genome influences methane emissions. In the present study, methane emissions were measured using a GreenFeed system in beef-on-dairy cattle ( = 11). High-throughput RNA sequencing was conducted on animal blood samples, followed by differential gene expression analysis using methane production (g/d) as a continuous trait. The analysis identified eleven differentially expressed genes (DEGs), including six downregulated (, , , , , ) and five upregulated (, , , , ) genes (adj < 0.05) with one gene exhibiting potential biomarker characteristics. Gene and cell enrichment, as well as pathway analysis, suggested that nervous, immune, and endocrine systems may be involved in ruminal methane production by beef-on-dairy cattle. These findings highlight the potential of transcriptomic biomarkers to guide genetic selection strategies, offering a sustainable pathway to reduce methane emissions and enhance both environmental and agricultural efficiency. - Source: PubMed
Publication date: 2026/02/13
Razban VahidCarballo Omar CristobalMorrison StevenShirali Masoud - Low birth weight in newborns is of multifactorial origin (fetal, maternal, placental, and environmental factors), and in one-third of cases, the cause is of unknown origin, with high infant morbidity and mortality. The main treatment for regaining weight and height in children with low birth weight is the application of growth hormones. However, their role as a protective factor to prevent an increase in body composition and the development of metabolic diseases is still poorly understood. : A case-control study was conducted in a cohort of patients consulted at the CES Pediatric Endocrinology Clinic, Medellín, Colombia, between 2008 and 2018. We evaluated sociodemographic and clinical variables. Additionally, the identification of differential patterns of genomic methylation between cases (treated with growth hormone) and controls (without growth hormone treatment) was performed. The groups were compared using Fisher's exact test for qualitative variables and Student's -test for the difference in means in independent samples. The correlation was evaluated with the Pearson coefficient. Regarding clinical manifestations, body mass index (BMI) was higher in children who did not receive growth hormone treatment, higher doses of growth hormone treatment helped reduce body mass index (R: -0.21, and = 0.067), and the use of growth hormone was related to a decrease in triglyceride blood concentrations ( = 0.06); these results tended towards significance. Regarding genome-wide methylation patterns, the following genes were found to be hypermethylated: , and . Meanwhile, the following genes were found hypomethylated: , and . Using growth hormone as a treatment in SGA newborns helps regain weight and height. Additionally, it could be a protective factor against the increase in adolescent body composition. - Source: PubMed
Publication date: 2025/05/23
Velásquez Juan M AlfaroVásquez Trespalacios Elsa MariaUrrego RodrigoArroyave Toro María CMontilla Velásquez María Del PilarSoto Cecilia Maria DíazVélez Juan C ZuluagaJaramillo Henríquez VerónicaFlórez Jorge Emilio SalazarMonroy Fernando PPalacio Mosquera Hernando AlirioVélez Gómez SaraPelaez Sánchez Ronald Guillermo