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Human Polyclonal ADCYAP1 Primary Antibody pour ELISA, WB - ABIN4343354
Bourgault, Vaudry, Botia, Couvineau, Laburthe, Vaudry, Fournier: Novel stable PACAP analogs with potent activity towards the PAC1 receptor. dans Peptides 2008
PACAP stimulates secretoneurin release and secretogranin II gene transcription in bovine adrenochromaffin cells
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.
PACAP stimulation promoted apoptosis by increasing Bax and decreasing Bcl2 expression.
Investigation of the mechanism of action suggested that a PACAP metabolite, identified as PACAP(9-38), might indeed be responsible for the observed PACAP38 antibacterial action. Surprisingly, PACAP(9-38), which does not induce haemolysis, exhibits an increased specificity toward Burkholderia cenocepacia J2315 compared to other tested bacteria.
PACAP can help to preserve the integrity of the newly synthetized cartilage matrix via signaling mechanisms, which ultimately inhibit the activity of matrix destroying enzymes under cellular stress.
The release of biologically active PACAP was described in mast cells; providing a potential biological explanation for the association between allergy and migraine.
that perturbations in the PACAP-PAC1R pathway may be involved in amyotrophic lateral sclerosis 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.
human migraine models have shed light on the importance of PACAP38 in the pathophysiology of primary headaches
PACAP stimulated repairing of corneal endothelium lesion as shown by wound healing analysis.
Studies suggest that the level of stress and circulating gonadal hormones may differentially regulate the PACAPergic system in males and females to influence anxiety-like behavior and may be one mechanism underlying the discrepancies in human psychiatric disorders. [Review Article]
Study indicates that both exogenous and endogenous pituitary adenylate cyclase activating polypeptide plays a regulatory role in small intestinal cells, but this is restricted to certain conditions, such as type of stressor and timing of application.
Some abnormalities of the PACAP system are evident in the brains of Sudden Infant Death Syndrome infants.
Study found that interictal serum PACAP levels are not increased (or decreased) in a large series of chronic migraine women when compared to matched controls without a headache history
Study found a protective effect of PACAP-38 on oxidative stress damage in zebrafish hair cells, suggesting PACAP-38 ability to prevent hair cells from apoptosis. PACAP-38 treatment decreased the cleaved caspase-3 level in the hair cells, but somewhat unexpectedly had no influence on p-38 MAPK pathway. PACAP-38 treatment also rescued H2O2-induced reduction in movement.
An association was found in a common variant of the PACAP receptor in patients with cluster headache.
It has potent neuroprotective and neuroregenerative functions. (review)
PACAP-38 is released in plasma during attacks of episodic cluster headache patients.
Hypermethylation of ADCYAP1 gene may be highly associated with the development of cervical cancer.
This review provides an overview of current knowledge regarding the neuroprotective effects, mechanisms of action, and therapeutic potential of PACAP in response to ischemic brain injuries
PACAP is involved in the pathogenesis of migraine rather than tension-type headache
PACAP38-PAC1 signaling process initiates bone marrow-derived cells homing into the ischemic brain for reducing brain injury.
Gene expression of PACAP-27 is stimulated across the thalamic paraventricular nucleus following alcohol drinking.
endogenous PACAP protects the brain of adolescent and adult mice from alcohol toxicity and modulates distinct sets of genes according to the maturation status of the brain.
Targeted deletion of pituitary adenylate cyclase-activating polypeptide (PACAP) from the ventral premamillary nucleus of the hypothalamus (PMV) led to delayed puberty onset and impaired reproductive function in female.
the results demonstrated that autophagy is induced in Parkinson's disease experimental models and that PACAP exhibits not only anti-apoptotic but also anti-autophagic properties.
Results show that lack of pituitary adenylate cyclase-activating polypeptide (PACAP) influences molecular and biomechanical properties of bone matrix, activating various signalling cascade changes in a compensatory fashion.
Low PACAP expression is associated with increased number of severely damaged sperms.
results suggest that IL-6 gene requires up-regulation of phospho-JAK2/STAT3, PACAP, and PAC1R and down-regulation of the TNF-alpha gene to modulate its anticonvulsive/neuroprotective potential
The data presented here shows PACAP38 transport is temporally altered following controlled cortical impact -treatment and PACAP38 uptake is greater in the cerebellum compared to the cortices
In conclusion, Pituitary adenylate cyclase activating polypeptidecan attenuate Mitoxantrone -mediated left ventricular dilation and dysfunction in mice.
This study shown the model of depression in PACAP mutation mice.
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.
Results suggests that PACAP regulates a bidirectional interaction between the adult neural progenitor cells and their niche: PACAP modifies extracellular matrix production and remodeling, in turn the extracellular matrix regulates progenitor cell adherence. PACAP may in this manner help restrict adult neural progenitors to the stem cell niche in vivo.
age-related changes were observed in the PACAP KO mice only. These alterations included horizontal and rod bipolar cell dendritic sprouting into the photoreceptor layer and decreased ganglion cell number. Also, Muller glial cells showed elevated GFAP expression compared to the aging WT retinas.
Mice lacking endogenous PACAP have slower weight gain during the first weeks of development and slower neurobehavioral development.
Study investigated effects of chronic variable mild stress (CVMS) in non-injected, vehicle and imipramine-treated KO mice vs. wildtype (WT) counterparts and mapped the CVMS-related FosB response in 18 brain areas; found that PACAP deficiency affects neuronal reactivity in a brain area-specific manner in stress centers
Backup mechanisms maintain PACAP/VIP-induced arterial vasodilation in PACAP-deficient mice.
PACAP/PAC1 signaling has a role in light regulated food anticipatory activity
PACAP deficient mice exhibit attenuated acute restraint stress response and chronic restraint stress response.
not only homozygous but also heterozygous PACAP deficient mice are more vulnerable to kidney ischemia/reperfusion, further supporting the nephroprotective effects of the endogenous PACAP
PACAP expression in the dorsal root ganglion following spinal nerve injury is controlled through transcriptional repressor, REST.
The temporal and spatial expression pattern of the ghrh-pacap1 transcript suggests that thise hormones may modulate patterning during development.
signal pathways, transcript distribution, and splice variants are investigated
expression of transcripts for PACAP and its receptors by 0.5-6 hpf make both PACAP1 and PACAP2 candidates for factors that influence brain development
study reveals the distribution of immunoreactive GHRH-like peptide in structures of the zebrafish brain; results suggest involvement of GHRH-LP in both neuroendocrine and feeding-associated nervous circuits
This gene encodes a secreted proprotein that is further processed into multiple mature peptides. These peptides stimulate adenylate cyclase and increase cyclic adenosine monophosphate (cAMP) levels, resulting in the transcriptional activation of target genes. The products of this gene are key mediators of neuroendocrine stress responses. Alternative splicing results in multiple transcript variants.
glucagon family neuropeptides
, growth hormone-releasing hormone
, pituitary adenylate cyclase-activating polypeptide
, pituitary adenylate cyclase activating polypeptide
, adenylate cyclase activating peptide, pituitary 1
, adenylate cyclase activating polypeptide 1 (pituitary)
, pituitary adenylate cyclase activating polypeptide 1
, pituitary adenylate cyclase-activating polypeptide precursor (Pacap)
, pituitary adenylate cyclase activating polypeptide, PACAP