MAPK3 & ARRB2 Protein Protein Interaction Antibody Pair
- Known as:
- MAPK3 & ARRB2 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0065
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAPK3 & ARRB2 Protein Interaction Antibody Pair
Related genes to: MAPK3 & ARRB2 Protein Protein Interaction Antibody Pair
- 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:
- MAPK3 NIH gene
- Name:
- mitogen-activated protein kinase 3
- Previous symbol:
- PRKM3
- Synonyms:
- ERK1, p44mapk, p44erk1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2015-09-03
Related products to: MAPK3 & ARRB2 Protein Protein Interaction Antibody Pair
Related articles to: MAPK3 & ARRB2 Protein Protein Interaction Antibody Pair
- Activation of CB by exogenous agonists causes adverse effects in vivo. Positive allosteric modulation may offer improved therapeutic potential and a reduced on-target adverse effect profile compared with orthosteric agonists, due to reduced desensitisation/tolerance, but this has not been directly tested. This study investigated the ability of PAMs/ago-PAMs to induce receptor regulation pathways, including desensitisation and receptor internalisation. - Source: PubMed
Publication date: 2024/06/03
Green Hayley MManning Jamie JGreig Ian RRoss Ruth AFinlay David BGlass Michelle - Caffeine has been extensively studied in the context of CNS pathologies as many researchers have shown that consuming it reduces pro-inflammatory biomarkers, potentially delaying the progression of neurodegenerative pathologies. Several lines of evidence suggest that adenosine receptors, especially A and AA receptors, are the main targets of its neuroprotective action. We found that caffeine pretreatment 15 min before LPS administration reduced the expression of Il1b in the hippocampus and striatum. The harmful modulation of caffeine-induced inflammatory response involved the downregulation of the expression of AA receptors, especially in the hippocampus. Caffeine treatment alone promoted the downregulation of the adenosinergic receptor Adora2A; however, this promotion effect was reversed by LPS. Although administering caffeine increased the expression of the enzymes DNA methyltransferases 1 and 3A and decreased the expression of the demethylase enzyme Tet1, this effect was reversed by LPS in the hippocampus of mice that were administered Caffeine + LPS, relative to the basal condition; no significant differences were observed in the methylation status of the promoter regions of adenosine receptors. Finally, the bioinformatics analysis of the expanded network demonstrated the following results: the Adora2B gene connects the extended networks of the adenosine receptors Adora1 and Adora2A; the Mapk3 and Esr1 genes connect the extended Adora1 network; the Mapk4 and Arrb2 genes connect the extended Adora2A network with the extended network of the proinflammatory cytokine Il1β. These results indicated that the anti-inflammatory effects of acute caffeine administration in the hippocampus may be mediated by a complex network of interdependencies between the Adora2B and Adora2A genes. - Source: PubMed
Publication date: 2024/03/15
Lemes Dos Santos Sanna PaulaBernardes Carvalho LiebertCristina Dos Santos Afonso Camilade Carvalho KassiaAires RogérioSouza JennyfferRodrigues Ferreira MarcelBirbrair AlexanderMartha Bernardi MariaLatini AlexandraFoganholi da Silva Rodrigo A - Arrestins were initially identified for their role in homologous desensitization and internalization of G protein-coupled receptors. Receptor-bound arrestins also initiate signaling by interacting with other signaling proteins. Arrestins scaffold MAPK signaling cascades, MAPK kinase kinase (MAP3K), MAPK kinase (MAP2K), and MAPK. In particular, arrestins facilitate ERK1/2 activation by scaffolding ERK1/2 (MAPK), MEK1 (MAP2K), and Raf (MAPK3). However, the structural mechanism underlying this scaffolding remains unknown. Here, we investigated the mechanism of arrestin-2 scaffolding of cRaf, MEK1, and ERK2 using hydrogen/deuterium exchange-mass spectrometry, tryptophan-induced bimane fluorescence quenching, and NMR. We found that basal and active arrestin-2 interacted with cRaf, while only active arrestin-2 interacted with MEK1 and ERK2. The ATP binding status of MEK1 or ERK2 affected arrestin-2 binding; ATP-bound MEK1 interacted with arrestin-2, whereas only empty ERK2 bound arrestin-2. Analysis of the binding interfaces suggested that the relative positions of cRaf, MEK1, and ERK2 on arrestin-2 likely facilitate sequential phosphorylation in the signal transduction cascade. - Source: PubMed
Qu ChangxiuPark Ji YoungYun Min WooHe Qing-TaoYang FanKim KiaeHam DongheeLi Rui-RuiIverson T MGurevich Vsevolod VSun Jin-PengChung Ka Young - 5-HTR, 5-HTR, and 5-HTR are three constitutively active G-coupled 5-HT receptors that have key roles in brain development, learning, memory, cognition, and other physiological processes in the central nervous system. In addition to G signaling cascade mediated by these three 5-HT receptors, the ERK1/2 signaling which is dependent on cyclic adenosine monophosphate (cAMP) production and protein kinase A (PKA) activation downstream of G signaling has also been widely studied. In this study, we investigated these two signaling pathways originating from the three G-coupled 5-HT receptors in AD293 cells. We found that the phosphorylation and activation of ERK1/2 are ligand-induced, in contrast to the constitutively active G signaling. This indicates that G signaling alone is not sufficient for ERK1/2 activation in these three 5-HT receptors. In addition to G, we found that β-arrestin and Fyn are essential for the activation of ERK1/2. Together, these results put forth a novel mechanism for ERK1/2 activation involving the cooperative action of G, β-arrestin, and Fyn. - Source: PubMed
Publication date: 2019/03/04
Liu PingYin Yu-LingWang TingHou LiWang Xiao-XiWang ManZhao Guan-GuanShi YiXu H EricJiang Yi - End-stage renal disease (ESRD) is the final stage of chronic kidney disease in which the kidney is not sufficient to meet the needs of daily life. It is necessary to understand the role of genes expression involved in ESRD patient responses to nocturnal hemodialysis (NHD) and to improve the immunity responsiveness. The aim of this study was to investigate novel immune-associated genes that may play important roles in patients with ESRD.The microarray expression profiles of peripheral blood in patients with ESRD before and after NHD were analyzed by network-based approaches, and then using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway analysis to explore the biological process and molecular functions of differentially expressed genes. Subsequently, a transcriptional regulatory network of the core genes and the connected transcriptional regulators was constructed. We found that NHD had a significant effect on neutrophil activation and immune response in patients with ESRD.In addition, Our findings suggest that MAPKAPK3, RHOA, ARRB2, FLOT1, MYH9, PRKCD, RHOG, PTPN6, MAPK3, CNPY3, PI3KCG, and PYGL genes maybe potential targets regulated by core transcriptional factors, including ARNT, C/EBPalpha, CEBPA, CREB1, PSG1, DAND5, SP1, GATA1, MYC, EGR2, and EGR3. - Source: PubMed
Dai HongweiZhou JiaoZhu Bo