Phospholipase C Activation by VIP1 and VIP2 Receptors Expressed in COS 7 Cells Involves a Pertussis Toxin-Sensitive Mechanism

MacKenzie, Cameron A.; Lutz, Eve M.; McCulloch, Derek; Mitchell, Rory; Harmar, Anthony J.

doi:10.1111/j.1749-6632.1996.tb17523.x

Cited by 27 publications

(22 citation statements)

References 10 publications

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“…As mentioned above, in addition to Gα s coupling leading to the activation of adenylate cyclase and subsequent cAMP production, VIP receptors are also able to activate PLC in a partly PTx (pertussis toxin)-sensitive manner [18,14]. However, PTx-sensitive mechanisms leading to PLC activation are different for VPAC1 and VPAC2.…”

Section: Signalling Pathwaysmentioning

confidence: 98%

Molecular mechanisms involved in vasoactive intestinal peptide receptor activation and regulation: current knowledge, similarities to and differences from the A family of G-protein-coupled receptors

Langer

Robberecht

2007

Biochemical Society Transactions

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An actual paradigm for activation and regulation of the GPCR (G-protein-coupled receptors)/seven-transmembrane helix family of receptors essentially emerges from extensive studies of the largest family of receptors, the GPCR-A/rhodopsin family. The mechanisms regulating the GPCR-B family signal transduction are less precisely understood due in part to the lack of the conserved signatures of the GPCR-A family (E/DRY, NPXXY) and in part to the absence of a reliable receptor modelling, although some studies suggest that both families share similar features. Here, we try to highlight the current knowledge of the activation and the regulation of the VIP (vasoactive intestinal peptide) receptors, namely VPAC (VIP/pituitary adenylate cyclase-activating peptide receptor) 1 and 2. This includes search for amino acids involved in the stabilization of the receptor active conformation and in coupling to G-proteins, signalling pathways activated in response to VIP, agonist-dependent receptor down-regulation, phosphorylation and internalization as well as pharmacological consequences of receptor hetero-dimerization.

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Section: Signalling Pathwaysmentioning

confidence: 98%

Molecular mechanisms involved in vasoactive intestinal peptide receptor activation and regulation: current knowledge, similarities to and differences from the A family of G-protein-coupled receptors

Langer

Robberecht

2007

Biochemical Society Transactions

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“…However, the precise mechanisms which contribute to VIP-induced [Ca 2 + ] i increase remain unclear due to divergent results. Indeed, in transfected cell lines some studies observed that activation of PLC was partly sensitive to pertussis toxin (PTx; MacKenzie et al, 1996; Langer et al, 2002), thus involving both Gαi and Gαq coupling, while others did not observe coupling to Gαi (Sreedharan et al, 1994). Moreover, PTx sensitive mechanisms leading to PLC activation seems different for VPAC 1 and VPAC 2 receptors.…”

Section: Signaling Pathways Activated By Vpac Receptorsmentioning

confidence: 99%

Mechanisms involved in VPAC receptors activation and regulation: lessons from pharmacological and mutagenesis studies

Langer

2012

Front. Endocrin.

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Vasoactive intestinal peptide (VIP) plays diverse and important role in human physiology and physiopathology and their receptors constitute potential targets for the treatment of several diseases such as neurodegenerative disorder, asthma, diabetes, and inflammatory diseases. This article reviews the current knowledge regarding the two VIP receptors, VPAC1 and VPAC2, with respect to mechanisms involved in receptor activation, G protein coupling, signaling, regulation, and oligomerization.

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“…However, a more recent study has shown that VIP protects rat myenteric neurones from the lethal effect of peritoneal mast cell degranulation [37], and taken together these studies suggest that VIP may have inhibitory or excitatory effects on mast cells, although in both cases the action of VIP occurred via VPAC2 only. The amino acid structure of VIP released by mast cells also differs from the common mammalian VIP structure, with a reported variation of the classical VIP(1-28) amino acid structure to a truncated VIP (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) produced by murine peritoneal mast cells, bone marrow derived mast cells and in rat basophilic leukaemia cells [38]. It has been shown that when murine mast cells are cultured with immunoglobulin (Ig)E, this stimulates the release of truncated VIP(10-28) together with histamine [38].…”

Section: Mast Cellsmentioning

confidence: 99%

Immunomodulation of innate immune responses by vasoactive intestinal peptide (VIP): its therapeutic potential in inflammatory disease

Smalley

Barrow

Foster

2009

Clinical and Experimental Immunology

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Summary Since the late 1970s a number of laboratories have studied the role of vasoactive intestinal peptide (VIP) in inflammation and immunity. These studies have highlighted the dramatic effect of VIP on immune cell activation and function, and studies using animal models of disease have indicated that VIP has significant therapeutic and prophylactic potential. This review will focus on the effects of VIP on innate immune cell function and discuss the therapeutic potential for VIP in inflammatory diseases of humans.

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Phospholipase C Activation by VIP1 and VIP2 Receptors Expressed in COS 7 Cells Involves a Pertussis Toxin-Sensitive Mechanism

Cited by 27 publications

References 10 publications

Molecular mechanisms involved in vasoactive intestinal peptide receptor activation and regulation: current knowledge, similarities to and differences from the A family of G-protein-coupled receptors

Molecular mechanisms involved in vasoactive intestinal peptide receptor activation and regulation: current knowledge, similarities to and differences from the A family of G-protein-coupled receptors

Mechanisms involved in VPAC receptors activation and regulation: lessons from pharmacological and mutagenesis studies

Immunomodulation of innate immune responses by vasoactive intestinal peptide (VIP): its therapeutic potential in inflammatory disease

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