ARL8A (Human) Recombinant Protein (P02)
- Known as:
- ARL8A (Human) Recombinant Protein (P02)
- Catalog number:
- H00127829-P02-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ARL8A (Human) Recombinant Protein (P02)
Related genes to: ARL8A (Human) Recombinant Protein (P02)
- 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
- Gene:
- HMCN2 NIH gene
- Name:
- hemicentin 2
- Previous symbol:
- -
- Synonyms:
- DKFZp434P0216, FLJ23816
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-03
- Date modifiied:
- 2018-11-16
- Gene:
- KCTD10 NIH gene
- Name:
- potassium channel tetramerization domain containing 10
- Previous symbol:
- -
- Synonyms:
- MSTP028, BTBD28
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-28
- Date modifiied:
- 2019-02-21
- Gene:
- RGPD4 NIH gene
- Name:
- RANBP2 like and GRIP domain containing 4
- Previous symbol:
- -
- Synonyms:
- RGP4, DKFZp686P0288
- Chromosome:
- 2q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-15
- Date modifiied:
- 2019-02-18
- Gene:
- WIPI2 NIH gene
- Name:
- WD repeat domain, phosphoinositide interacting 2
- Previous symbol:
- -
- Synonyms:
- ATG21, CGI-50, FLJ12979, FLJ14217, FLJ42984, DKFZP434J154, DKFZp686P02188, ATG18B
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-15
- Date modifiied:
- 2016-03-01
Related products to: ARL8A (Human) Recombinant Protein (P02)
Related articles to: ARL8A (Human) Recombinant Protein (P02)
- 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. - 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 - Triple-negative breast cancer (TNBC) is a major concern among the different subtypes of breast cancer (BC) due to the lack of effective treatment. In a previous study by our group aimed at understanding the difference between TNBC and non-TNBC tumors, we identified the gene TBC1 domain family member 9 (), the expression of which was lower in TNBC as compared to non-TNBC tumors. In the present study, analysis of TBC1D9 expression in TNBC ( = 58) and non-TNBC ( = 25) patient tumor samples validated that TBC1D9 expression can differentiate TNBC (low) from non-TNBC (high) samples and that expression of TBC1D9 was inversely correlated with grade and proliferative index. Moreover, we found that downregulation of the gene decreases the proliferation marginally in non-TNBC and was associated with increased migratory and tumorigenic potential in both TNBC and luminal BC cell lines. This increase was mediated by the upregulation of , , , , , and expression in TBC1D9 knockdown cells. Our results suggest that TBC1D9 expression might limit tumor aggressiveness and that it has a differential expression in TNBC vs. non-TNBC tumors. - Source: PubMed
Publication date: 2021/07/16
Kothari CharuClemenceau AlissonOuellette GenevièveEnnour-Idrissi KaoutarMichaud AnnickC-Gaudreault RenéDiorio CarolineDurocher Francine