Recombinant Taricha granulosa Cannabinoid receptor 1 (CNR1)

Lyophilized powder
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Avoid repeated freeze-thaw cycles. Store working aliquots at 4°C for up to one week.

Centrifuge the vial briefly before opening to collect the contents. Reconstitute the protein in sterile deionized water to a concentration of 0.1-1.0 mg/mL. For long-term storage, we recommend adding 5-50% glycerol (final concentration) and aliquoting at -20°C/-80°C. Our standard glycerol concentration is 50% and can serve as a guideline.

Shelf life depends on storage conditions, buffer composition, temperature, and protein stability. Generally, liquid formulations have a 6-month shelf life at -20°C/-80°C, while lyophilized forms have a 12-month shelf life at -20°C/-80°C.

Store at -20°C/-80°C upon receipt. Aliquot for multiple uses to prevent repeated freeze-thaw cycles.

Tag type is determined during manufacturing.
The specific tag type is finalized during production. Please indicate your preferred tag type for prioritized development.

Tris/PBS-based buffer, 6% Trehalose.

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1-473

full length protein

Taricha granulosa (Roughskin newt)

CNR1

MKSILDGLADTTFRTITTDLLYMGSNDVQYEDTKGEMASKLGYFPQKLPLSSFRRDHSPD KMTIGDDNLLSFYPLDQFNVTEFFNRSVSTFKENDDNLKCGENFMDMECFMILTASQQLI IAVLSLTLGTFTVLENFLVLCVILQSRTLRCRPSYHFIGSLAVADLLGSVIFVYSFLDFH VFHRKDSSNVFLFKLGGVTASFTASVGSLFLTAIDRYISIHRPLAYKRIVTRTKAVIAFC VMWTIAIIIAVLPLLGWNCKKLKSVCSDIFPLIDENYLMFWIGVTSILLLFIVYAYVYIL WKAHSHAVRMLQRGTQKSIIIHTSEDGKVQITRPEQTRMDIRLAKTLVLILVVLIICWGP LLAIMVYDVFGKMNNPIKTVFAFCSMLCLMDSTVNPIIYALRSQDLRHAFLEQCPPCEGT SQPLDNSMESDCQHRHGNNAGNVHRAAENCIKSTVKIAKVTMSVSTETSGEAV

Q9PUI7

The cannabinoid receptor 1 (CNR1) is a G-protein coupled receptor that binds to cannabinoids, including endocannabinoids such as N-arachidonoylethanolamide (anandamide or AEA) and 2-arachidonoylglycerol (2-AG). It mediates various cannabinoid effects, influencing appetite, memory, gastrointestinal motility, catalepsy, locomotor activity, anxiety, and chronic pain. Signal transduction typically involves a decrease in cyclic AMP. In the hypothalamus, CNR1 exhibits a dose-dependent, potentially cell-type-specific, dual effect on mitochondrial respiration: stimulating respiration at low doses and inhibiting it at high doses. At high doses, signaling involves G-protein alpha-i subunit activation, subsequent inhibition of mitochondrial soluble adenylate cyclase, reduced cyclic AMP levels, and inhibition of protein kinase A (PKA)-dependent phosphorylation of mitochondrial electron transport chain subunits (e.g., NDUFS2). In the hypothalamus, it inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increases in SREBF1 and FASN gene expression. Following cannabinoid activation, it promotes food intake by stimulating the release of orexigenic beta-endorphin from hypothalamic POMC neurons, without affecting melanocyte-stimulating hormone alpha/alpha-MSH release. In the hippocampus, it regulates cellular respiration and energy production in response to cannabinoids. CNR1 is involved in depolarization-induced suppression of inhibition (DSI), where depolarization of CA1 pyramidal neurons releases eCBs that activate presynaptic CB1 receptors, transiently reducing GABAergic inhibition. It also modulates excitatory synaptic transmission. In superior cervical ganglia and cerebral vascular smooth muscle cells, it constitutively and agonist-dependently inhibits voltage-gated Ca(2+) channels. CNR1 increases leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidneys, contributing to hyperleptinemia. In adipose tissue, CNR1 signaling increases SREBF1, ACACA, and FASN gene expression. In the liver, cannabinoid activation increases de novo lipogenesis and reduces fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB, and FASN genes. It may also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. CNR1 peripherally modulates energy metabolism. In high-carbohydrate diet-induced obesity, it may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase (DLD) in striated muscles, along with certain glucose/pyruvate metabolic enzymes, impacting energy expenditure through mitochondrial metabolism. Anandamide activation of CNR1 elicits a proinflammatory response in macrophages, involving NLRP3 inflammasome activation and IL1B and IL18 secretion.

G-protein coupled receptor 1 family

Cell membrane; Multi-pass membrane protein. Mitochondrion outer membrane. Cell projection, axon. Cell junction, synapse, presynapse.