C1orf102 Blocking Peptide
- Known as:
- C1orf102 Blocking Peptide
- Catalog number:
- 33r-1480
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- C1orf102 Blocking Peptide
Related genes to: C1orf102 Blocking Peptide
- 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 Blocking Peptide
Related articles to: C1orf102 Blocking Peptide
- 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 - Alveolar bone loss is a main manifestation of periodontitis. Human periodontal ligament stem cells (PDLSCs) are considered as optimal seed cells for alveolar bone regeneration due to its mesenchymal stem cell like properties. Osteogenic potential is the premise for PDLSCs to repair alveolar bone loss. However, the mechanism regulating osteogenic differentiation of PDLSCs remain elusive. In this study, we identified Neuron-derived orphan receptor 1 (NOR1), was particularly expressed in PDL tissue in vivo and gradually increased during osteogenic differentiation of PDLSCs in vitro. Knockdown of NOR1 in hPDLSCs inhibited their osteogenic potential while NOR1 overexpression reversed this effect. In order to elucidate the downstream regulatory network of NOR1, RNA-sequencing was used. We found that downregulated genes were mainly enriched in TGF-β, Hippo, Wnt signaling pathway. Further, by western blot analysis, we verified that the expression level of phosphorylated-SMAD2/3 and phosphorylated-SMAD4 were all decreased after NOR1 knockdown. Additionally, ChIP-qPCR and dual luciferase reporter assay indicated that NOR1 could bind to the promoter of TGFBR1 and regulate its activity. Moreover, overexpression of TGFBR1 in PDLSCs could rescue the damaged osteogenic potential after NOR1 knockdown. Taken together, our results demonstrated that NOR1 could activate TGF-β/SMAD signaling pathway and positively regulates the commitment of osteoblast lineages of PDLSCs by targeting TGFBR1 directly. - Source: PubMed
Publication date: 2024/08/09
Wu YunJing HuanLi YicunLi MengqingZheng YatingLin YuntaoMa GuixingCao HuilingYang Hongyu - Oxidored-nitro domain-containing protein 1 (NOR1) is a critical tumour suppressor gene, though its regulatory mechanism in oxidative stress of glioblastoma (GBM) remains unclear. Hence, further study is needed to unravel the function of NOR1 in the progression of oxidative stress in GBM. In this study, we evaluated the expression of NOR1 and nuclear respiratory factor 1 (NRF1) in GBM tissue and normal brain tissue (NBT) using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB), and investigated their relationship. We then induced oxidative stress in U251 cells through H2O2 treatment and conducted Cell Count-ing Kit-8, Transwell and wound healing assays to analyse cell proliferation, invasion and migration. Cell apoptosis was assessed by flow cytometry and TUNEL staining. We also measured the activities of superoxide dismutase and catalase, as well as the level of reactive oxygen species (ROS) using biochemical techniques. Via qRT-PCR and WB, the mRNA and protein expression levels of NOR1 and NRF1 were determined. Chromatin immunoprecipitation (ChIP) assays were applied to validate NRF1's interaction with NOR1. Our results showed that the expression of NOR1 and NRF1 was low in GBM, and their expression levels were positively correlated. H2O2-induced oxidative stress reduced NRF1 and NOR1 expression levels and increased the ROS level. The ChIP assay confirmed the binding of NRF1 to NOR1. Over-expression of NRF1 attenuated the inhibitory effect of oxidative stress on the proliferation, migration and invasion of U251 cells, which was reversed by knockdown of NOR1. - Source: PubMed
Wang JialiChen ShuaiXiang WangZhu QingRen Nianjun