ARRB2 Antibody (monoclonal) (M01)
- Known as:
- ARRB2 Antibody (mab) (M01)
- Catalog number:
- AT1201a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ARRB2 Antibody (monoclonal) (M01)
Related genes to: ARRB2 Antibody (monoclonal) (M01)
- Gene:
- ARRB2 NIH gene
- Name:
- arrestin beta 2
- Previous symbol:
- ARR2
- Synonyms:
- BARR2, DKFZp686L0365
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-10
- Date modifiied:
- 2016-10-05
- Gene:
- GTF2H2B NIH gene
- Name:
- general transcription factor IIH subunit 2B (pseudogene)
- Previous symbol:
- -
- Synonyms:
- DKFZP686M0199
- Chromosome:
- 5q13.2
- Locus Type:
- pseudogene
- Date approved:
- 2008-07-04
- Date modifiied:
- 2015-11-09
- Gene:
- POLR1A NIH gene
- Name:
- RNA polymerase I subunit A
- Previous symbol:
- -
- Synonyms:
- DKFZP586M0122, FLJ21915, RPO1-4, RPA1
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2017-06-28
- Gene:
- TDRP NIH gene
- Name:
- testis development related protein
- Previous symbol:
- C8orf42
- Synonyms:
- INM01, TDRP1, TDRP2
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2015-08-26
Related products to: ARRB2 Antibody (monoclonal) (M01)
Related articles to: ARRB2 Antibody (monoclonal) (M01)
- Altered detection and preference for sodium are associated with increased sodium intake, and increased sodium intake is associated with increased risk of hypertension. ATR (angiotensin II type 1 receptor) second-messenger signaling is mediated and modulated by ARRB2 (β-arrestin-2), and both ATR and ARRB2 in the brain influence sodium intake. Here, we examined the hypotheses that ARRB2 influences sodium taste hedonics and that these effects involve ATR. - Source: PubMed
Publication date: 2026/06/01
Grobe Connie CHamilton Autumn JTreesukosol YadaGrobe Justin LSegar Jeffrey LSigmund Curt D - Arrestins regulate G protein-coupled receptor (GPCR) signaling by undergoing large-scale conformational rearrangements, yet the solution-state equilibria that underlie arrestin pre-activation remain poorly defined. While prior studies identified slow conformational exchange at the interdomain interface, these minor states could not be structurally linked to activation because their resonances broaden beyond detection upon receptor binding. Here, we use multinuclear NMR spectroscopy to characterize the intrinsic conformational landscape of full-length, human arrestin-2 in solution. We identify two distinct, pre-existing conformational equilibria that mirror key steps of the receptor-driven activation process. First, a slow exchange process populates a receptor-bound-like, interdomain-twisted conformation at physiological temperatures. In parallel, a faster, globally distributed equilibrium populates a state consistent with C-terminal tail release. Dynamic analyses reveal localized rigidification in the receptor-bound-like minor states despite arrestin's overall flexibility, while backbone relaxation data indicate widespread μs-ms conformational exchange. Together, these results demonstrate that arrestin-2 acts as a preorganized scaffold that intrinsically samples receptor-binding relevant conformations in the absence of binding partners. This provides a solution-state framework for arrestin pre-activation and establishes a dynamic fingerprint for future ligand-dependent studies. - Source: PubMed
Shriver Tucker JKahraman KeremPan MingzheDağ ÇağdaşTonelli MarcoRobson Scott AZiarek Joshua J - Archaic introgression has shaped the modern human immune system, particularly components involved in RNA virus responses. In contrast, its contribution to DNA virus defense remains poorly understood. Here, we investigate the contribution of Neandertal- and Denisovan-introgressed haplotypes to viral load of five common DNA viruses in UK Biobank samples, using genome-wide association summary statistics. We identified 18 genome-wide significant associations, predominantly involving Epstein-Barr virus (EBV) and loci within the Major Histocompatibility Complex, including a Denisovan-like haplotype tightly linked to HLA-A*11:01. Notably, the archaic alleles of these haplotypes showed a directional bias toward increased viral loads. Focusing on two chromosome 17 haplotypes associated with higher EBV load, we identified phenotypic associations with blood cell traits and disease markers, as well as functional effects on immune-relevant genes, including GSDMB, ARRB2, and ALOX15. Allele frequency analysis of one of the chromosome 17 haplotypes revealed signatures of shifting modes of selection, possibly reflecting changes in pathogen landscapes over time. Our results suggest that archaic DNA systematically contributes to DNA virus immunity in modern humans, with effects distinct from previously described RNA virus associations. These findings provide novel evolutionary and functional insights into host-virus interactions and the role of archaic admixture in antiviral defense. - Source: PubMed
Rajpara RutviPolishchuk Sofiia StefaniiaYermakovich DanatDannemann Michael - Hepatic ischemia-reperfusion injury (IRI) is an important factor affecting the prognosis of liver transplantation patients. The role of Arrb2 in liver injury is unclear. Our study aimed to determine the role of Arrb2 in hepatic IRI and to identify its underlying mechanisms. - Source: PubMed
Publication date: 2026/04/24
Wang Xiao-WenZheng Wen-JieChen Hao-QiHuang TaoZhang YuanYan Xi-JingLi Wen-ChaoZou LongWu Jie-ZhongZhu Wen-FengYang Qi-WeiWang Gen-ShuHu Kun-Peng - Intrahepatic cholangiocarcinoma (ICC) is a major contributor to cancer-related mortality on a global scale, yet it suffers from a lack of reliable early diagnostic biomarkers and effective therapeutic targets. Pemigatinib has been identified as a therapeutic option for advanced ICC; however, its long-term clinical efficacy is significantly hindered by the development of drug resistance. To address this, pemigatinib-resistant ICC cells were established by culturing with increasing drug treatment. 98 pairs of ICC tissue samples were collected and analyzed to assess the association between β-arrestin 2 (ARRB2) and ICC progression. The role and mechanism of ARRB2 in the malignant progression of ICC and resistance to pemigatinib were explored in vitro and in vivo experiments. The results demonstrated that ARRB2 expression is markedly upregulated in pemigatinib-resistant ICC cells compared to their parental counterparts. Suppression of ARRB2 expression markedly attenuated ICC chemoresistance to pemigatinib. Clinical data further verified that ARRB2 is correlated with poorer pathological stage and prognosis in ICC patients. Mechanistic studies revealed that ARRB2 activation in ICC is mediated by METTL3-dependent m6A methylation. Functional analyses demonstrated that ARRB2 promotes the malignant progression of ICC by facilitating YAP nuclear translocation while also modulating the sensitivity of ICC to pemigatinib through the Raf-MEK-ERK signaling axis. This study identifies the tumor-promoting activities of ARRB2 and elucidates the regulatory mechanism of the METTL3-ARRB2-YAP/Raf axis in ICC, which may provide a novel prognostic biomarker and potential therapeutic target for human ICC. - Source: PubMed
Publication date: 2026/04/15
Chen HaoqiWang XiaowenZhu WenfengZheng WenjieYang QiweiLiang ZhixingZhang YuanLi XuejiaoLiang JinliangChen XiaolongLi HuaYe LinsenLi HuiYan XijingZhu ShuguangWang Genshu