Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.4.3 (
phospholipase C
)
18,461
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Asthma is an inflammatory disease in which proinflammatory cytokines have a role in inducing abnormalities of airway smooth muscle function and in the development of airway hyperresponsiveness. Inflammatory cytokines alter calcium (Ca
2+
) signaling and contractility of airway smooth muscle, which results in nonspecific airway hyperresponsiveness to agonists. In this context, Ca
2+
regulatory mechanisms in airway smooth muscle and changes in these regulatory mechanisms encompass a major component of airway hyperresponsiveness. Although dynamic Ca
2+
regulation is complex,
phospholipase C
/inositol tris-phosphate (PLC/IP3) and
CD38
-cyclic ADP-ribose (
CD38
/cADPR) are two major pathways mediating agonist-induced Ca
2+
regulation in airway smooth muscle. Altered
CD38
expression or enhanced cyclic ADP-ribosyl cyclase activity associated with
CD38
contributes to human pathologies such as asthma, neoplasia, and neuroimmune diseases. This review is focused on investigations on the role of
CD38
-cyclic ADP-ribose signaling in airway smooth muscle in the context of transcriptional and posttranscriptional regulation of
CD38
expression. The specific roles of transcription factors NF-kB and AP-1 in the transcriptional regulation of
CD38
expression and of miRNAs miR-140-3p and miR-708 in the posttranscriptional regulation and the underlying mechanisms of such regulation are discussed.
...
PMID:CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms. 2957 47
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