Anti-CNR1 Antibody (2Z39)

Name: Anti-CNR1 Antibody (2Z39)
Brand: TargetMol
SKU: TMAH-00289
Rating: 4.5 (1 reviews)

还可以

产品编号 TMAH-00289

Anti-CNR1 Antibody (2Z39) 是一种抗体，靶向 CNR1。Anti-CNR1 Antibody (2Z39) 可用于 ELISA。

Anti-CNR1 Antibody (2Z39)

还可以

产品编号 TMAH-00289

Anti-CNR1 Antibody (2Z39) 是一种抗体，靶向 CNR1。Anti-CNR1 Antibody (2Z39) 可用于 ELISA。

规格	价格	库存	数量
50 μL	¥ 1,300	5日内发货
100 μL	¥ 2,190	5日内发货

大包装 & 定制

加入购物车

TargetMol 的所有产品仅用作科学研究或药证申报，不能被用于人体，我们不向个人提供产品和服务。请您遵守承诺用途，不得违反法律法规规定用于任何其他用途。

实验操作小课堂

常见问题解答

联系我们获取更多批次信息

资源下载

产品操作手册

产品介绍

生物活性

产品描述	Anti-CNR1 Antibody (2Z39) is an antibody targeting CNR1. Anti-CNR1 Antibody (2Z39) can be used in ELISA.
Ig Type	Human IgG4(S228P)
克隆号	2Z39
交叉反应	Human
验证活性	The Binding Activity of Huamn CNR1 with Anti-CNR1 recombinant Antibody Activity: Measured by its binding ability in a functional ELISA. Immobilized Human CNR1 at 10 μg/mL can bind Anti-CNR1 recombinant antibody, the EC50 is 41.72-63.54 ng/mL.
应用	ELISA
抗体种类	Monoclonal
亚细胞定位	Cell membrane; Multi-pass membrane protein. Membrane raft. Mitochondrion outer membrane. Cell projection, axon. Cell junction, synapse, presynapse.
构建方式	Recombinant Antibody
纯化方式	Affinity-chromatography
性状	Liquid
缓冲液	Preservative: 0.03% Proclin 300. Constituents: 50% Glycerol, 0.01M PBS, PH 7.4.
研究背景	G-protein coupled receptor for endogenous cannabinoids (eCBs), including N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG), as well as phytocannabinoids, such as delta(9)-tetrahydrocannabinol (THC). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP. In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission. In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner. In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca(2+) channels leads to vasodilation and decreased vascular tone. Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes. In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism. In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism. In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion. In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells. Binds both 2-AG and anandamide. Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 2 in assays measuring GTP binding to membranes. Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 3 in assays measuring GTP binding to membranes.