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CGRP Antibody [N20P10]

Cat.No.: F1470

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IF1:1600

Application
WB, IF

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
5 kDa

Datasheet & SDS

Biological Description

Specificity
CGRP Antibody [N20P10] detects endogenous levels of total CGRP protein.

Clone
N20P10

Synonym(s)
CALCA; Calcitonin gene-related peptide 1; CGRP1; Alpha-type CGRP; Calcitonin gene-related peptide I (CGRP-I); CALC1

Background
CGRP (calcitonin gene-related peptide), primarily in the form of α-CGRP from the CALCA gene and β-CGRP from CALCB, is a 37-amino-acid neuropeptide characterized by a critical N-terminal disulfide-bonded ring (Cys²–Cys⁷) required for receptor activation, an α-helical segment (residues 8–18) for high-affinity binding, a flexible β-turn (residues 19–26), and a C-terminal amide (Phe³⁷) that anchors the peptide to the extracellular domain of the CGRP receptor. This receptor is a heterodimeric family B GPCR complex composed of the calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein 1 (RAMP1), with receptor component protein (RCP) facilitating Gs protein coupling. Upon CGRP binding, the CLR/RAMP1 complex undergoes conformational changes that increase cAMP via adenylyl cyclase activation, leading to PKA-mediated phosphorylation of CREB, KATP channels, and ERK1/2, which together drive vasodilation (through NO/PKG/eNOS signaling and smooth muscle hyperpolarization), neurogenic inflammation (mast cell degranulation and cytokine release), and pain sensitization (by enhancing TRPV1 channels in nociceptors). In the two-domain binding model, the C-terminal region docks to the receptor’s extracellular domain, positioning the disulfide loop and Thr⁶ for engagement with transmembrane and extracellular loop regions, thereby amplifying downstream signaling, while RAMP1 modulates ligand affinity and specificity. CGRP is pivotal in migraine pathogenesis via dural vasodilation and positive feedback on CGRP release, confers cardioprotection through ischemic preconditioning and IP3R modulation, and modulates neuromuscular and synaptic activity. Dysregulation of CGRP contributes to migraine (with levels rising during attacks and targeted by monoclonal antibodies like erenumab), cluster headaches, and neuropathic pain, while receptor antagonists (gepants) leverage its receptor signaling bias for therapeutic benefit without affecting calcitonin-induced hypotension.

Background

CGRP (calcitonin gene-related peptide), primarily in the form of α-CGRP from the CALCA gene and β-CGRP from CALCB, is a 37-amino-acid neuropeptide characterized by a critical N-terminal disulfide-bonded ring (Cys²–Cys⁷) required for receptor activation, an α-helical segment (residues 8–18) for high-affinity binding, a flexible β-turn (residues 19–26), and a C-terminal amide (Phe³⁷) that anchors the peptide to the extracellular domain of the CGRP receptor. This receptor is a heterodimeric family B GPCR complex composed of the calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein 1 (RAMP1), with receptor component protein (RCP) facilitating Gs protein coupling. Upon CGRP binding, the CLR/RAMP1 complex undergoes conformational changes that increase cAMP via adenylyl cyclase activation, leading to PKA-mediated phosphorylation of CREB, KATP channels, and ERK1/2, which together drive vasodilation (through NO/PKG/eNOS signaling and smooth muscle hyperpolarization), neurogenic inflammation (mast cell degranulation and cytokine release), and pain sensitization (by enhancing TRPV1 channels in nociceptors). In the two-domain binding model, the C-terminal region docks to the receptor’s extracellular domain, positioning the disulfide loop and Thr⁶ for engagement with transmembrane and extracellular loop regions, thereby amplifying downstream signaling, while RAMP1 modulates ligand affinity and specificity. CGRP is pivotal in migraine pathogenesis via dural vasodilation and positive feedback on CGRP release, confers cardioprotection through ischemic preconditioning and IP3R modulation, and modulates neuromuscular and synaptic activity. Dysregulation of CGRP contributes to migraine (with levels rising during attacks and targeted by monoclonal antibodies like erenumab), cluster headaches, and neuropathic pain, while receptor antagonists (gepants) leverage its receptor signaling bias for therapeutic benefit without affecting calcitonin-induced hypotension.

References
https://pubmed.ncbi.nlm.nih.gov/25287861/ https://pubmed.ncbi.nlm.nih.gov/23186257/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%