Rabbit Link
- Known as:
- Rabbit Link
- Catalog number:
- M 004
- Product Quantity:
- 100ml
- Category:
- -
- Supplier:
- Diagnostic Biosystems
- Gene target:
- Rabbit Link
Related genes to: Rabbit Link
- Gene:
- RAPGEFL1 NIH gene
- Name:
- Rap guanine nucleotide exchange factor like 1
- Previous symbol:
- -
- Synonyms:
- Link-GEFII
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-01
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Link
(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (R - sr, pl), Host Rabbit, Extraction-free, CE-marked Related articles to: Rabbit Link
- - Source: PubMed
Publication date: 2026/03/02
Skalski MarcinKowal-Wiśniewska EwelinaJaskiewicz-Rajewicz KatarzynaKiwerska KatarzynaBartochowska AnnaUstaszewski AdamGórecki TomaszMajchrzak-Celińska AleksandraWierzbicka MałgorzataJarmuż-Szymczak MałgorzataPaluszczak Jarosław - Biological sex has been shown to influence aging outcomes, contributing to distinct trajectories in disease susceptibility and lifespan. DNA methylation patterns provide a quantitative measure of biological aging. This study investigated whether aged male and female mice display distinct liver DNA methylation patterns and differences in epigenetic aging. Liver samples were collected from 17 aged c57BL/6 mice (6 males, 11 females). Genomic DNA was extracted and bisulfite-converted before targeted enrichment of 2,045 murine age-associated CpG loci. Biological age (DNAge) was estimated using a previously developed DNA methylation-based predictor generated through elastic net regression. The difference (ΔDNAge) between DNAge and chronological age was computed. Sex-specific differences were assessed by comparing site-specific methylation ratios, ΔDNAge values, and through principal component analysis (PCA) and multiple linear regression. Twelve CpG sites across six genes (, , , , , and ) showed significant sex-associated differences in methylation. demonstrated the largest and most consistent sex-associated effect, with all three associated CpG sites showing higher methylation in males (regression coefficients: -0.204, -0.281, and -0.294). exhibited consistent lower methylation ratios in females, whereas the other genes showed higher methylation in females. There were no sex differences in biological age or ΔDNAge ( = 0.596). Although the epigenetic clock did not reveal differences between sexes in aging, aged mice did exhibit sex-specific liver methylation patterns different from those reported in younger mice, suggesting that sex-dependent epigenetic changes may emerge later in life and may reflect sexual dimorphism in liver function with age. Males and females are known to age differently and develop certain diseases at different rates. Here, we examined the livers of aged male and female mice to see if they show different DNA methylation patterns. We found that aged male and female mice had distinct DNA methylation patterns at specific genes. Interestingly, most of these methylation differences were not present in younger mice, suggesting that sex differences in the genome may change with age. - Source: PubMed
Publication date: 2026/02/16
Apelian ShantMamillapalli RamanaiahUcar AbdullahGawde NimishaTaylor Hugh S - Non-alcoholic fatty liver disease (NAFLD), recently retermed as metabolic dysfunction-associated steatotic liver disease (MASLD), and intervertebral disc degeneration (IVDD) are major health burdens with rising prevalence. Despite affecting different organ systems, emerging evidence suggests potential molecular crosstalk between these conditions. However, the underlying mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/01/26
Wang GuohaoLiu YongmingShen Xingchao - Melanoma, a highly heterogeneous malignancy, remains refractory to conventional therapies due to poorly defined molecular and metabolic drivers. Short-chain fatty acid (SCFA) metabolism influences tumor progression, yet its role in melanoma subtypes and clinical outcomes is unclear. This study aims to delineate melanoma subgroups driven by SCFA metabolic dysregulation and identify mechanisms underlying their aggressiveness. - Source: PubMed
Publication date: 2025/10/01
Fang YongjinXu XiaofanLu RihuiHuang YeDai XinshenHuang PuchengFu XuefengZhuge Pan - Among endocrine cancers, thyroid carcinoma (TC) is the most prevalent and ranks sixth in global mortality rates. Aberrant expression of long non-coding RNA (lncRNAs) is associated with the progression of various human cancers, including TC. The role of PICSAR lncRNA (LINC00162) has been validated in different human cancers. Therefore, this study aimed to assess the expression levels and functions of lncRNA PICSAR in thyroid cancer tumorigenesis. This comprehensive approach combined in silico and in vitro methods to explore the molecular mechanisms and clinical significance of PICSAR in thyroid cancer. This work assessed the expression of the long non-coding RNA LINC00162 and identified differentially expressed genes (DEGs) using the Cancer Genome Atlas (TCGA) database. Interactions among LINC00162, hsa-miR-320A, hsa-miR-485, and RAPGEFL1 were investigated using the LncACT and miRDB databases. Bioinformatics techniques were employed to conduct functional enrichment analysis to clarify the relevant molecular pathways. For the investigation of LINC00162 expression in TC samples, 50 matched samples of thyroid carcinoma and adjacent normal tissue were gathered. Real time PCR was used to objectively evaluate the expression levels of the targeted genes. Every tissue sample was examined pathologically. A specific siRNA was transfected into a thyroid cancer cell line to examine the functional role of LINC00162. The impact of LINC00162 silencing was then assessed by measuring the level of target genes expression following the transfection. Based on TCGA-THCA analysis and qRT-PCR on tissue samples, LINC00162 (PICSAR) was markedly overexpressed in thyroid cancer tissues compared to normal samples. However, no discernible correlation was found between LINC00162 expression and the pathological characteristics of thyroid cancer. Our bioinformatics predictions based on lncRNA-microRNA interactions demonstrate that LINC00162 acts as a molecular sponge for the downregulated microRNAs hsa-miR-320A and hsa-miR-485 in thyroid cancer. RAPGEFL1, a gene associated with the development of thyroid cancer, is upregulated in conjunction with this downregulation. The LINC00162-miRNA-RAPGEFL1 axis is involved in critical carcinogenic processes, including thiamine metabolism, cell cycle control, and folate biosynthesis, according to functional enrichment analysis. Additionally, a bioinformatics study revealed a negative association between PICSAR and the NUDT3 gene, while a positive correlation was found with the SNX18P14 gene. Thyroid cancer cells transfected with LINC00162-specific siRNA showed significant downregulation of LINC00162 and RAPGEFL1, alongside an increase in hsa-miR-320A and hsa-miR-485, ultimately inhibiting the growth of thyroid cancer. These findings suggest that targeting PICSAR may offer a treatment strategy for thyroid cancer by altering important biological processes. In conclusion, LINC00162, which is overexpressed in thyroid cancer, acts as a molecular sponge for hsa-miR-320A and hsa-miR-485, regulating key oncogenic pathways and leading to the upregulation of RAPGEFL1. These effects are reversed upon siRNA-mediated silencing of LINC00162, indicating its potential as a promising therapeutic target for thyroid cancer. RAPGEFL1 regulates the Rap signaling pathway, controlling adhesion, migration, polarity, and metabolism to maintain cellular and tissue homeostasis. Its dysregulation is linked to various diseases, highlighting its potential as a therapeutic target. - Source: PubMed
Publication date: 2025/08/26
Hejazi MaryamJafari TahminehYari AmirHosseinHeshmat RaminLarijani BagherAhvaz SamanehPourbagherian OmidTavangar Seyed MohammadShafiee GitaMokhtarzadeh Amir Ali