EFCAB4B Blocking Peptide
- Known as:
- EFCAB4B Blocking Peptide
- Catalog number:
- 33r-4566
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- EFCAB4B Blocking Peptide
Related genes to: EFCAB4B Blocking Peptide
- Gene:
- CRACR2A NIH gene
- Name:
- calcium release activated channel regulator 2A
- Previous symbol:
- EFCAB4B
- Synonyms:
- MGC4266
- Chromosome:
- 12p13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-21
- Date modifiied:
- 2015-08-24
Related products to: EFCAB4B Blocking Peptide
Related articles to: EFCAB4B Blocking Peptide
- - Source: PubMed
Publication date: 2025/04/21
Lee JinguBalzraine BrettSchweizer AlexisKuzmanova VasilisaGwack YousangRazani BabakLee Jin-MooMosher Deane FCho Jaehyung - The role of calcium release-activated calcium channel (CRAC) inhibitors in the pathogenesis of rheumatoid arthritis (RA) is unclear. We focused on stromal interaction molecule 1 (STIM1) and Ca release-activated channel regulator 2 A (CRACR2A), which participate in CRAC activation, to understand the signaling mechanism of human RA fibroblast-like synovial (FLS) cells in response to shear stress (SS). Human normal and RA FLS cell cultures were studied. The rates of intracellular calcium release and extracellular calcium influx in response to SS differed, and the responses to the first and second stimuli were analyzed. In the RA FLS cells, CRAC inhibitor significantly decreased the second/first stimulus ratio compared with that of the normal cells, and STIM1 and CRACR2A exhibited significantly increased expression levels compared with those in the normal FLS cells. Therefore, STIM1 and CRACR2A expression and Ca influx in FLS cells are implicated in the pathogenesis of RA. - Source: PubMed
Publication date: 2025/03/06
Okumura YuHonoki KanyaTanaka YasuhitoTakaki MiyakoAsada Keiji - is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of variants in the progression of non-alcoholic fatty liver disease (NAFLD). In this study we show that mice with global depletion of have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis of liver tissues to investigate differential global gene expression among and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes ( and ) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with . - Source: PubMed
Publication date: 2025/02/15
Cheng Chew WPedicini LuciaAlcala Cintli MoralesDeligianni FeniaSmith JessicaMurray Ryan DTodd Harriet JForde NiamhMcKeown Lynn - Ca release-activated Ca channel regulator 2A (CRACR2A) has been linked to immunodeficiency attributable to T-cell dysfunction in humans. We discovered that neutrophil CRACR2A promotes neutrophil adhesive and migratory functions by facilitating Ca mobilization and β2 integrin activation. - Source: PubMed
Publication date: 2024/11/27
Lee JinguBalzraine BrettSchweizer AlexisKuzmanova VasilisaGwack YousangRazani BabakLee Jin-MooMosher Deane FCho Jaehyung - Mast cells are infamous for mediating allergic and inflammatory diseases due to their capacity of rapidly releasing a wide range of inflammatory mediators stored in cytoplasmic granules. However, mast cells also have several important physiological roles that involve selective and agonist-specific release of these active mediators. While a filtering mechanism at the plasma membrane could regulate the selective release of some cargo, the plethora of stored cargo and the diversity of mast cell functions suggests the existence of granule subtypes with distinct trafficking pathways. The molecular mechanisms underlying differential trafficking and exocytosis of these granules are not known, neither is it clear how granule trafficking is coupled to the stimulus. In endothelial cells, a Rab GTPase, Rab46, responds to histamine but not thrombin signals, and this regulates the trafficking of a subpopulation of endothelial-specific granules. Here, we sought to explore, for the first time, if Rab46 plays a role in mast cell function. We demonstrate that Rab46 is highly expressed in human and murine mast cells, and Rab46 genetic deletion has an effect on mast cell degranulation that depends on both stimuli and mast cell subtype. This initial insight into the contribution of Rab46 to mast cell function and the understanding of the role of Rab46 in stimuli-dependent trafficking in other cell types necessitates further investigations of Rab46 in mast cell granular trafficking so that novel and specific therapeutic targets for treatment of the diverse pathologies mediated by mast cells can be developed. - Source: PubMed
Publication date: 2023/12/22
Pedicini LuciaSmith JessicaSavic SinisaMcKeown Lynn