ARL8A Antibody
- Known as:
- ARL8A Antibody
- Catalog number:
- 36138
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- ARL8A Antibody
Related genes to: ARL8A Antibody
- Gene:
- ARL8A NIH gene
- Name:
- ADP ribosylation factor like GTPase 8A
- Previous symbol:
- ARL10B
- Synonyms:
- FLJ45195, Gie2
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-05
- Date modifiied:
- 2015-11-19
Related products to: ARL8A Antibody
Related articles to: ARL8A Antibody
- Average daily gain (ADG), age at 115 kg (AGE), backfat thickness (BF), and loin eye area (LEA) are key growth and carcass traits in pigs. However, breed-specific molecular regulatory mechanisms underlying these traits remain largely unknown. Here, we identified multiple candidate genes associated with these 4 traits from Duroc and Yorkshire pigs by three Genome-wide association study(GWAS) methods (MLM, FarmCPU, and BLINK) and differential genes expression analysis, verified them based on RNA sequencing(RNA-seq), Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq), and Chromatin Immunoprecipitation sequencing (ChIP-seq) data from Duroc and Yorkshire pigs, and explored the regulatory mechanisms underlying these traits. - Source: PubMed
Publication date: 2026/05/25
Zhao AnyangQiao JiakunKuang RenzhuoChen ZiyiTan YunruZhu MengjinZhou Guangliang - BACKGROUND: Although previous studies have linked colorectal cancer (CRC) with lipid metabolism and inflammatory signaling, the specific roles of phosphatidylcholine metabolites and their interactions with inflammatory cytokines in the tumor microenvironment remain poorly understood. METHODS: This study utilizes an integrated multi-omics analysis approach. We performed a two-sample Mendelian randomization analysis using data from 1400 metabolites and 91 inflammatory cytokines to investigate their associations with CRC, followed by experimental validation of the findings. Single-cell transcriptomics revealed metabolic state differences, while machine learning constructed a predictive model. SHAP analysis interpreted the model, with spatial transcriptomics validating key findings. RESULTS: The phosphatidylcholine metabolite DPPC was identified as causally associated with CRC risk. Our results demonstrated DPPC promotes tumor progression by inhibiting TNFSF14 secretion. Our DPPC-based model effectively predicted CRC progression, with SHAP analysis identifying ARL8A, MTUS1, and TMEM184A as key contributors. These findings were validated spatially and translated into a clinical nomogram for prognosis and immunotherapy guidance. In summary, this study highlights the significance of DPPC-mediated regulation within the tumor microenvironment in predicting CRC progression and guiding potential therapeutic strategies. - Source: PubMed
Publication date: 2026/01/02
Li XingDong HaifengJin ZihanYu HongZhou HaoChen JingyaoWang ChenChen SongyaoZhang ChanghuaChen Hengxing - Bipolar disorder is a mood-related disorder, which can be portrayed as extreme shifts in energy, mood, and activity levels which can also be characterized by manic highs and depressive lows that can be often misdiagnosed as unipolar disorder due to primitive diagnostics techniques based on clinical assessments as well as diagnostic complexities arising due to its heterogeneous nature and overlapping symptoms with conditions like schizophrenia. leading to delays in treatment Strong evidence in support of genetic and epigenetic aspects of bipolar disorder, including mechanisms such as compromised hypothalamic-pituitary-adrenal axis, immune-inflammatory imbalances, oxidative stress, and mitochondrial dysfunction are found. Moreover, some previous research has already stated the role of genes like CITED2, NUDT4, and Arl8B in these processes. The primary goal of this study is to investigate the involvement of the genes in exploring and validating their potential as biomarkers for bipolar disorder. In silico tools like MutationTaster, PolyPhen2, SIFT, GTEx, PhenoScanner, and RegulomeDB were used to perform mutational and gene expression analyses. Results revealed potentially dangerous mutations caused in CITED2, NUDT4, and Arl8B, those which can have diverse outcomes. RegulomeDB, GTEx, and PhenoScanner reveal the involvement of these genes in various brain regions highlighting their relevance to bipolar disorder. This analysis suggests the potential utility of CITED2, NUDT4, and Arl8B as diagnostic markers hence shedding light on their roles to elaborate the molecular range of bipolar disorder. The study also contributes to providing valuable insights into the genetic and molecular basis of bipolar disorders. - Source: PubMed
Publication date: 2024/09/18
Maheshwari HarshitaGarg PrekshiSrivastava Prachi - The genome-wide association studies (GWAS) analysis, the most successful technique for discovering disease-related genetic variation, has some statistical concerns, including multiple testing, the correlation among variants (single-nucleotide polymorphisms) based on linkage disequilibrium and omitting the important variants when fitting the model with just one variant. To eliminate these problems in a small sample-size study, we used a sparse Bayesian learning model for finding bipolar disorder (BD) genetic variants. - Source: PubMed
Publication date: 2023/12/31
Kazemi Naeini MaryamAkbarzadeh MahdiKazemi IrajSpeed DougHosseini Sayed Mohsen - When intracellular, pathogenic Salmonella reside in a membrane compartment composed of interconnected vacuoles and tubules, the formation of which depends on the translocation of bacterial effectors into the host cell. Cytoskeletons and their molecular motors are prime targets for these effectors. In this study, we show that the microtubule molecular motor KIF1Bβ (a splice variant of KIF1B), a member of the kinesin-3 family, is a key element for the establishment of the Salmonella replication niche as its absence is detrimental to the stability of bacterial vacuoles and the formation of associated tubules. Kinesin-3 interacts with the Salmonella effector SifA but also with SKIP (also known as PLEKHM2), a host protein complexed to SifA. The interaction with SifA is essential for the recruitment of kinesin-3 on Salmonella vacuoles whereas that with SKIP is incidental. In the non-infectious context, however, the interaction with SKIP is essential for the recruitment and activity of kinesin-3 only on a fraction of the lysosomes. Finally, our results show that, in infected cells, the presence of SifA establishes a kinesin-1 and kinesin-3 recruitment pathway that is analogous to and functions independently of that mediated by the Arl8a and Arl8b GTPases. This article has an associated First Person interview with the first author of the paper. - Source: PubMed
Publication date: 2022/01/10
Fang ZiyanFallet MathieuMoest ThomasGorvel Jean-PierreMéresse Stéphane