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Bat Polyclonal Vip Primary Antibody for IEM, ICC - ABIN617890
Schultea, Dees, Ojeda: Postnatal development of sympathetic and sensory innervation of the rhesus monkey ovary. in Biology of reproduction 1993
Show all 501 Pubmed References
Human Polyclonal Vip Primary Antibody for IF (p), IHC (p) - ABIN724565
Wieck, El-Nachef, Hou, Spurrier, Holoyda, Schall, Garcia Mojica, Collins, Trecartin, Cheng, Frykman, Grikscheit: Human and Murine Tissue-Engineered Colon Exhibit Diverse Neuronal Subtypes and Can Be Populated by Enteric Nervous System Progenitor Cells When Donor Colon Is Aganglionic. in Tissue engineering. Part A 2015
Cow (Bovine) Polyclonal Vip Primary Antibody for IHC (p) - ABIN2477078
Stojsic, Brasanac, Bilanovic, Mitrovic, Stevanovic, Boricic: Large-cell neuroendocrine carcinoma of the ampulla of Vater. in Medical oncology (Northwood, London, England) 2010
Human Polyclonal Vip Primary Antibody for IHC (p) - ABIN4886760
Huang, Zhu, Zhang, Zhu, Liu, Zhu, Wang, Li, Yang, Dong, Liu, Chen, Zhang, Yang, Deng, Fan, Wang, Liu, Ma, Fu, Wu: S100+ cells: a new neuro-immune cross-talkers in lymph organs. in Scientific reports 2013
VIP SNPs are associated with VIP serum level and response to rheumatoid arthritis treatment.
this review provides an overview of VIP effects on rheumatoid arthritis pathology
Results have suggested that pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP), but predominantly VIP, induce neuroblastoma differentiation into benign form by regulating hypoxia-inducible factors, vascular endothelial growth factor and vascular endothelial growth factor receptor expression and distribution.
Results found that VIP enhanced trophoblast cell migration and invasion through the activation of high affinity VPAC receptors and PKA-CRE signaling pathways suggesting that VIP-mediated autocrine pathways regulate trophoblast cell function and contribute to immune homeostasis maintenance at placentation.
this study shows that that VIP exerts anti-inflammatory effects by inhibiting the MAPK-p47phox phosphorylation-NOX2 activation axis, and that VIP dampens carrageenan-induced inflammation in rats
Both mast cells and VIP appear to be important factors in the regulation of this bacterial translocation through the colonic mucosa of irritable bowel syndrome patients.
we found that VIP inhibits NFAT nuclear translocation in primary human pulmonary artery smooth muscle cells (PASMC). Early activation of NFATc3 in IPF patients may contribute to disease progression and the increase in VIP expression could be a protective compensatory mechanism
VIP and CRF reduce ADAMTS expression and function in osteoarthritis synovial fibroblasts.
optogenetically activating single VIPs in live mice while recording the activity of nearby neurons, we find that VIPs break open a hole in blanket inhibition.
a differential effect of VIP on the expression of TNFalpha and IL-6 receptors, since VIP was only able to decreased expression in LPS-stimulated monocytes but not in 4/74-infected monocytes.
VIP promotes Th17 polarization of memory Th cells in early arthritis.
The circadian rhythm amplitude of motor activity in both Alzheimer disease subjects and age-matched controls is correlated with the number of vasoactive intestinal peptide-expressing suprachiasmatic nucleus neurons.
Skin VIP expression, a marker of sudomotor innervation, was significantly lower in patients with familial transthyretin amyloid neuropathy compared to controls.
Alterations in VIP expression may play a role in irritable bowel syndrome.
Interictal CGRP and, to a lesser degree, VIP levels measured in peripheral blood are of great help in predicting response of chronic migraine patients to Onabotulinumtoxin type A
The antimicrobial peptide, VIP is a neuropeptide with activity against a range of microorganisms from skin, oral, respiratory and gastrointestinal tract sites.
VIP is significantly increased in the patients with chronic obstructive pulmonary disease and pulmonary hypertension.
Serum levels of vasoactive intestinal peptide as a prognostic marker in early arthritis.
Data suggest that two closely related neuroprotective peptides, vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating peptide (PACAP), are up-regulated in neurons/immune cells after injury and/or inflammation. [REVIEW]
Our study suggested that baicalein exerts a positive effect on the VIP expression in HCMV-infected EVT at maternal-fetal interface.
Data show that PKA and PKC pathways are involved in the differential regulation of production of the neuropeptides (Met)enkephalin, galanin, somatostatin, NPY, and VIP.
The intestinal concentration of VIP increased gradually during development. The levels of VIP and VIPR1 in liver gradually decreased during development.
High level of co-expression of PACAP with VIP, SP and CGRP in the distal ganglia of the vagus sensory perikarya directly implicates studied peptides in their functional interaction during nociceptive vagal transduction.
The present study reports for the first time on the co-localisation of CART and VIP in myenteric neurons of the porcine transverse colon.
In vivo administration of lentivirus expressing VIP exerts a potent therapeutic effect on LPS-induced Acute Lung Injury in mice via inhibiting inflammation.
A significant myenteric neuronal cell loss and upregulation of VIP expression were found after focal, but not global, cerebral ischaemia.
Martinotti cells in layers II/III of the mouse primary somatosensory cortex are inhibited by both parvalbumin (PV)- and vasoactive intestinal polypeptide (VIP)-expressing cells.
BAD phosphorylation is essential in the cytoprotective effect of vasoactive intestinal peptide on cancer stem cells.
The suprachiasmatic nucleus (SCN)network consists of multiple clusters of cellular circadian rhythms that are differentially integrated by AVP and VIP signaling, depending on the postnatal period
PACAP/PAC1 signaling is important for light regulated behavior, VIP/VPAC2 signaling for stable clock function and both signaling pathways may play a role in shaping diurnality versus nocturnality.
The data of this study support a key role for VIP interneurons in cortical circuit development and suggest a possible contribution to pathophysiology in neurodevelopmental disorders
During arousal, VIP cells rapidly and directly inhibit pyramidal neurons; VIP cells also indirectly excite these pyramidal neurons via parallel disinhibition.
This study found that VIP-/- mice show a bilateral tactile hypersensitivity after spared nerve injury and a bilateral increase in neuronal activation upon innocuous tactile paw stimulation.
Several studies have shown that VIP(+) cells are sensitive to neuromodulation and increase their firing during locomotion, whisking, and pupil dilation and are involved in spatially specific top-down modulation, reminiscent of the effects of top-down attention, and also that attention enhances spatial resolution. Our findings provide a bridge between these studies by establishing the inhibitory circuitry that regulates th
majority of GnRH neurons in male and female mice express functional VIP receptors; effects of VIP on GnRH neurons do not alter across the estrous cycle
Backup mechanisms maintain PACAP/VIP-induced arterial vasodilation in PACAP-deficient mice.
in cortical VIP neurons, experience-dependent gene transcription regulates visual acuity by activating the expression of IGF1, thus promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons
Chronic loss of VIP in mice leads to a disruption of certain but not all immunological compartments.
neuropeptides CGRP and VIP have an important role in suppressing bone resorptive activities through RANKL/OPG pathway, similar to mechanical loading.
The results show in vivo a primary role for VIP chronic exposure in CFTR membrane stability and function and confirm in vitro data.
VIP signaling modulates the output from the olfactory bulb to maintain circadian rhythms in the mammalian olfactory system.
VIP neuropeptide-mediated cAMP-PKA signaling has an important role in hepatic homeostasis and cytoprotection in vivo
Loss of the VIP gene orchestrates a panoply of pathogenic genes which are detrimental to both left and right cardiac homeostasis.
Serum VIP was elevated significantly in the cholesterol gallstone groups compared to controls.
The protein encoded by this gene belongs to the glucagon family. It stimulates myocardial contractility, causes vasodilation, increases glycogenolysis, lowers arterial blood pressure and relaxes the smooth muscle of trachea, stomach and gall bladder. Alternative splicing occurs at this locus and two transcript variants encoding distinct isoforms have been identified.
, vasoactive intestinal polypeptide
, histidine-isoleucine/vasoactive intestinal polypeptide
, vasoactive intestinal polypeptide type I
, vasoactive intestinal peptide
, vasoactive instestinal peptide
, PHI, peptide histidine isoleucine