CALCB

更新于：2025-05-07

基本信息

别名

Beta-CGRP、Beta-type CGRP、CALC2

+ [6]

简介

CALCB/CGRP2 is a peptide hormone that induces vasodilation mediated by the CALCRL-RAMP1 receptor complex (PubMed:1318039, PubMed:9620797). Dilates a variety of vessels including the coronary, cerebral and systemic vasculature. Its abundance in the CNS also points toward a neurotransmitter or neuromodulator role (PubMed:3492492).

关联

100 项与 CALCB 相关的临床结果

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100 项与 CALCB 相关的转化医学

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0 项与 CALCB 相关的专利（医药）

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138

项与 CALCB 相关的文献（医药）

2025-04-01·Allergy

Human Pulmonary Neuroendocrine Cells Respond to House Dust Mite Extract With PAR‐1 Dependent Release of CGRP

Article

作者: Armbruster, Marie ; Puttagunta, Lakshmi ; Mandal, Shivani ; Forsythe, Paul ; Mann‐Nüttel, Ritu

ABSTRACTBackgroundPulmonary neuroendocrine cells (PNEC) are rare airway epithelial cells that have recently gained attention as potential amplifiers of allergic asthma. However, studying PNEC function in humans has been challenging due to a lack of cell isolation methods, and little is known about human PNEC function in response to asthma‐relevant stimuli. Here we developed and characterized an in vitro human PNEC model and investigated the neuroendocrine response to extracts of the common aeroallergen house dust mite (HDM).MethodsPNEC‐enriched cultures were generated from human induced pluripotent stem cells (iPNEC) and primary bronchial epithelial cells (ePNEC). Characterized PNEC cultures were exposed to HDM extract, a volatile chemical odorant (Bergamot oil), or the bacterial membrane component, lipopolysaccharide (LPS), and neuroendocrine gene expression and neuropeptide release determined.ResultsBoth iPNEC and ePNEC models demonstrated similar baseline neuroendocrine characteristics and a stimuli‐specific modulation of gene expression. Most notably, exposure to HDM but not Bergamot oil or LPS, leads to dose‐dependent induction of the CGRP encoding gene, CALCB, and corresponding release of the neuropeptide. HDM‐induced CALCB expression and CGRP release could be inhibited by a protease‐activated receptor 1 (PAR1) antagonist or protease inhibitors and was mimicked by a PAR1 agonist.ConclusionsWe have characterized a novel model of PNEC‐enriched human airway epithelium and utilized this model to demonstrate a previously unrecognized role for human PNEC in mediating a direct neuroendocrine response to aeroallergen exposure.

2024-12-01·Neurology Genetics

Shared Genetics of Migraine and Gastrointestinal Disorders Implicates Underlying Neurologic Mechanisms Yet Heterogeneous Etiologies

Article

作者: Chasman, Daniel I. ; Staller, Kyle ; Chan, Andrew T. ; Rist, Pamela M. ; Guo, Yanjun

Background and ObjectivesMigraine is strongly comorbid with irritable bowel syndrome (IBS), one of several gastrointestinal (GI) conditions that are distinguished by symptomatic profiles that are partly overlapping. Potential shared mechanisms of migraine and the GI conditions were investigated by assessing shared genetics on a genome-wide basis.MethodsAnalyses leveraged genome-wide summary statistics from large-scale genetic studies for migraine, including by aura status, IBS, peptic ulcer disease (PUD), gastrointestinal reflux (GERD), functional dyspepsia (FD), diverticular disease (DD), and the immune-related inflammatory bowel disease (IBD) or its constituents, ulcerative colitis (UC) and Crohn disease (CD). Genetic correlation was evaluated on a genome-wide basis and at independent local regions, including those related to therapeutic targeting of serotonin and the calcitonin gene-related peptide. Genetic correlation was assessed for enrichment at genes according to tissue specificity of gene expression. Potential causality between migraine and the GI conditions was assessed by Mendelian randomization.ResultsGenetic correlation with migraine was strongly significant among the nonimmune GI disorders, maximally for IBS (rg [SE] = 0.37[0.04], p = 10^-21) and minimally for DD (0.18 (0.04), 7.5 × 10^-7), but null for IBD. There were distinct patterns of local genetic sharing with migraine across the GI conditions at 22 significant segments of the genome, 7 of which were novel for either migraine or GI or both. Enrichment analysis suggested involvement of the CNS in genetic overlap of GERD, IBS, and PUD with migraine. There was local genetic sharing with migraine at CALCA/CALCB (encoding calcitonin gene-related peptide [CGRP]) in an inverse sense for GERD and PUD, but with concordance and greater significance for DD, IBD, and UC. Mendelian randomization supported causal effects of PUD, GERD and particularly DD (OR[SE] = 1.90 (1.35-2.68, p = 2.2 × 10^-4) on migraine, but not of migraine on any GI condition.DiscussionGenetic sharing of migraine and non-immune-related GI disorders was extensive yet distinct across GI disorders that have overlapping symptoms, with enrichment signals that imply neurologic mechanisms. Causal effects of some GI conditions on migraine were supported. A concordant local correlation at CALCA/CALCB of migraine with both DD and the immune-related disorders suggests potential benefit to these conditions from repurposed migraine therapeutics targeting CGRP.

2024-05-01·European Journal of Neuroscience

Characterizing enteric neurons in dopamine transporter (DAT)‐Cre reporter mice reveals dopaminergic subtypes with dual‐transmitter content

Article

作者: Gruenheid, Samantha ; Premachandran, Shobina ; Recinto, Sherilyn Junelle ; Yaqubi, Moein ; Mukherjee, Sriparna ; Stratton, Jo Anne ; Allot, Alexis ; MacDonald, Adam ; Trudeau, Louis‐Eric

AbstractThe enteric nervous system (ENS) comprises a complex network of neurons whereby a subset appears to be dopaminergic although the characteristics, roles, and implications in disease are less understood. Most investigations relating to enteric dopamine (DA) neurons rely on immunoreactivity to tyrosine hydroxylase (TH)—the rate‐limiting enzyme in the production of DA. However, TH immunoreactivity is likely to provide an incomplete picture. This study herein provides a comprehensive characterization of DA neurons in the gut using a reporter mouse line, expressing a fluorescent protein (tdTomato) under control of the DA transporter (DAT) promoter. Our findings confirm a unique localization of DA neurons in the gut and unveil the discrete subtypes of DA neurons in this organ, which we characterized using both immunofluorescence and single‐cell transcriptomics, as well as validated using in situ hybridization. We observed distinct subtypes of DAT‐tdTomato neurons expressing co‐transmitters and modulators across both plexuses; some of them likely co‐releasing acetylcholine, while others were positive for a slew of canonical DAergic markers (TH, VMAT2 and GIRK2). Interestingly, we uncovered a seemingly novel population of DA neurons unique to the ENS which was ChAT/DAT‐tdTomato‐immunoreactive and expressed Grp, Calcb, and Sst. Given the clear heterogeneity of DAergic gut neurons, further investigation is warranted to define their functional signatures and decipher their implication in disease.

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