The VIP2 antibody is a specialized immunological tool targeting the vasoactive intestinal peptide receptor 2 (VIPR2), also known as VPAC2. VIPR2 is a G protein-coupled receptor (GPCR) that binds vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP), playing critical roles in immune modulation, neuroprotection, and cancer progression . VIP2 antibodies are widely used to study receptor localization, signaling mechanisms, and therapeutic potential across diverse biological systems.
VIP2 antibodies are rigorously validated for specificity and functionality:
Specificity Testing: Antibodies such as Alomone Labs' Anti-VPAC2 (AVR-002) and Abcam’s ab154046 are validated using knockout models (Vipr2−/− mice) and preadsorption with blocking peptides .
Cross-Reactivity: These antibodies exhibit reactivity across human, rat, and mouse samples, confirmed via Western blot and flow cytometry .
Epitope Recognition: AVR-002 targets an extracellular N-terminal epitope (amino acids 25–37), enabling cell-surface detection in live cells .
VIP2 antibodies are employed across multiple experimental paradigms:
Western Blotting: Detects ~140 kDa bands in human Raji and K562 cell lysates .
Immunocytochemistry: Localizes VPAC2 in neuronal membranes (e.g., rat PC12 cells) .
Flow Cytometry: Identifies surface VPAC2 in live Jurkat T cells .
Breast Cancer: VIPR2 signaling promotes metastasis via PI3Kγ-driven PI(3,4,5)P3 synthesis, enhancing WAVE2-mediated actin remodeling .
Pancreatic Cancer: Autocrine VIP/VPAC2 signaling upregulates Piwil2 (a stem-cell protein) and TGFβ-1, driving tumor growth and immune evasion .
VIPR2 agonists (e.g., LBT-3627) reduce dopaminergic neuron loss in Parkinson’s models by suppressing microglial inflammation .
VPAC2 is highly expressed in the suprachiasmatic nucleus (SCN), regulating circadian rhythms .
VIPR2 activation inhibits NFκB and AP-1 in macrophages, reducing proinflammatory cytokines but increasing susceptibility to Salmonella infections .
In dendritic cells, VIPR2 signaling skews T-cell differentiation toward Th2 phenotypes .