Ask about this productRelated genes to: CAMLG antibody
- Gene:
- CAMLG NIH gene
- Name:
- calcium modulating ligand
- Previous symbol:
- -
- Synonyms:
- CAML, GET2
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-08
- Date modifiied:
- 2016-10-05
Related products to: CAMLG antibody
Related articles to: CAMLG antibody
- On a global scale, coronary artery disease (CAD) continues to be one of the leading causes of morbidity and death. Glycosylation, a vital post-translational modification, has been linked to a range of cardiovascular conditions, including CAD. This study aims to systematically identify and validate glycosylation-based prognostic biomarkers for CAD, with the ultimate goal of developing a novel clinical diagnostic tool. - Source: PubMed
Publication date: 2026/02/06
Fan KangjunWang MengZhang LinLi ZhaoshuiWang HongjingJiang Ting - Alternative splicing shapes isoform diversity and gene dosage but how genetic variation impacts splicing in brain disease is still not fully characterized. We assembled BigBrain, a multi-ancestry resource of 10,725 bulk RNA-seq profiles with matched genotypes from 4,656 individuals across 43 tissue-cohort pairs, and mapped 68,358 -sQTLs affecting 10,966 genes using mixed-model meta-analysis. Using SuSiE, we finemapped over half of these sQTLs into 95% credible sets, frequently to a single variant near splice sites. We further annotated variants predicted to alter dosage through frameshifts or nonsense-mediated decay or disrupt protein domains. Colocalization with seven neurodegenerative and psychiatric GWAS highlighted 97 loci where alternative splicing appears to mediate genetic risk. Among sQTL-eQTL pairs with colocalization probability ≥ 0.8 (posterior probability of a shared causal variant), half shared credible-set variants, showing that splicing can complement or act independently of expression. Mechanistic examples include (Parkinson's), (Schizophrenia), and (Alzheimer's). - Source: PubMed
Publication date: 2025/11/10
Réal AlineBp KailashDredge Winston HMuller Benjamin ZJang BeomjinTokolyi AlexWon Hong-HeeHumphrey JackRaj TowfiqueKnowles David A - Several genetic loci known to confer risk for Parkinson's disease (PD) function in lysosomal pathways. We systematically screened common variants linked to PD risk by genome-wide association studies (GWAS) for impact on cerebrospinal fluid (CSF) proteins reflecting lysosomal function. - Source: PubMed
Publication date: 2025/03/07
Zhang HanwenKargilis DanielTropea ThomasRobinson JohnShen JunchaoBrody Eliza MBrinkmalm AnnSjödin SimonBerndt Adama JCarceles-Cordon MarcSuh EunRanVan Deerlin Vivianna MBlennow KajWeintraub DanielLee Edward BZetterberg HenrikChen-Plotkin Alice S - Large case-control genome-wide association studies (GWASs) have detected loci associated with insomnia, but how these risk loci confer disease risk remains largely unknown. By integrating brain protein quantitative trait loci (pQTL) (N = 376, N = 152) and expression QTL (eQTL) (N = 452) datasets, with the latest insomnia GWAS summary statistics (N = 109,548, N = 277440), we conducted proteome/transcriptome-wide association study (PWAS/TWAS) and Mendelian randomization (MR) analysis, aiming to identify causal proteins involving in the pathogenesis of insomnia. We also explored the bi-directional causality between insomnia and several common diseases. As a result, the altered protein level of 28 genes in the brain was associated with the risk of insomnia in the discovery stage of PWAS, of which 18 genes' associations were replicated in the confirmatory stage of PWAS. Among them, four proteins (2-aminoethanethiol dioxygenase (ADO), calcium-modulating cyclophilin ligand (CAMLG), islet cell autoantigen 1 like (ICA1L) and latexin (LXN)) were found to be the most likely causal genes for insomnia with validations from TWAS, MR, and colocalization results. Specifically, the higher protein level of ADO, CALMG, and ICA1L was causally associated with a lower risk of insomnia. In comparison, the higher protein level of LXN was causally associated with an increased risk for insomnia. Moreover, genetically predicted insomnia was causally associated with an increased risk of developing cardiovascular diseases and depression. In conclusion, our study identified ADO, CAMLG, ICA1L, and LXN as potentially causal proteins in the pathogenesis of insomnia. This could provide insights into further mechanistic studies and therapeutic development for insomnia. - Source: PubMed
Publication date: 2025/01/18
Long JiangDou MengTang XiangdongGu Xiaojing - Biliverdin, a heme metabolite, has been previously reported to alleviate cerebral ischemic reperfusion injury (CIRI). However, the alterations of brain proteome profiles underlying this treatment remain elusive. The objective of this study is to analyze the differential protein expression profile in cerebral cortex of rats involved in anti-CIRI effects of Biliverdin, providing experimental foundation for searching specific marker proteins. Rat model of MCAO/R was established, HE staining, TTC staining, TUNEL staining, and neurological behavioral examination, corner turning test, adhesive removal test, were performed to validate the effects of Biliverdin, and the results indicated that Biliverdin plays a significant role in alleviating CIRI. Furthermore, proteomic analysis of brain tissues of rats subjected to CIRI following Biliverdin treatment was performed using an integrated TMT-based quantitative proteomic approach coupled with LC-MS/MS technology to clarify the comprehensive mechanisms of Biliverdin in CIRI. First, we conducted strict quality control data for TMT experiments. Finally, a total of 7366 proteins were identified, of which 95 proteins were differentially expressed (DEPs) between the CIRI group and the Sham group and 52 between the CIRI and BV groups. In addition, two overlapping proteins among the 147 DEPs, Atg4c and Camlg, were validated by RT-qPCR and western blotting, and their levels were consistent with the results of TMT analysis. Taken together, the current findings firstly mapped comprehensive proteomic changes after CIRI treated with Biliverdin, providing a foundation for developing potentially therapeutic targets of anti-CIRI of Biliverdin and clinically prognostic biomarkers of stroke. - Source: PubMed
Publication date: 2023/11/22
Bai WenyaHuo SiyingLi JunjieYang YuanZhou GuilinShao Jianlin