Results 31 to 40 of about 17,158 (246)

Apprehending the NAD+–ADPr-Dependent Systems in the Virus World

open access: yesViruses, 2022
NAD+ and ADP-ribose (ADPr)-containing molecules are at the interface of virus–host conflicts across life encompassing RNA processing, restriction, lysogeny/dormancy and functional hijacking.
Lakshminarayan M. Iyer   +3 more
doaj   +1 more source

Snake venom NAD glycohydrolases: primary structures, genomic location, and gene structure [PDF]

open access: yesPeerJ, 2019
NAD glycohydrolase (EC 3.2.2.5) (NADase) sequences have been identified in 10 elapid and crotalid venom gland transcriptomes, eight of which are complete.
Ivan Koludarov, Steven D. Aird
doaj   +2 more sources

Identification of a common non-apoptotic cell death mechanism in hereditary retinal degeneration. [PDF]

open access: yesPLoS ONE, 2014
Cell death in neurodegenerative diseases is often thought to be governed by apoptosis; however, an increasing body of evidence suggests the involvement of alternative cell death mechanisms in neuronal degeneration.
Blanca Arango-Gonzalez   +16 more
doaj   +1 more source

Roles of Nicotinamide Adenine Dinucleotide (NAD+) in Biological Systems

open access: yesChallenges, 2018
NAD+ has emerged as a crucial element in both bioenergetic and signaling pathways since it acts as a key regulator of cellular and organism homeostasis. NAD+ is a coenzyme in redox reactions, a donor of adenosine diphosphate-ribose (ADPr) moieties in ADP-
Palmiro Poltronieri, Nataša Čerekovic
doaj   +1 more source

Paracrine ADP Ribosyl Cyclase-Mediated Regulation of Biological Processes

open access: yesCells, 2022
ADP-ribosyl cyclases (ADPRCs) catalyze the synthesis of the Ca2+-active second messengers Cyclic ADP-ribose (cADPR) and ADP-ribose (ADPR) from NAD+ as well as nicotinic acid adenine dinucleotide phosphate (NAADP+) from NADP+. The best characterized ADPRC
Cecilia Astigiano   +7 more
doaj   +1 more source

CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms

open access: yesMediators of Inflammation, 2018
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.
Deepak A. Deshpande   +6 more
doaj   +1 more source

Enhanced sensitivity to cholera toxin in female ADP-ribosylarginine hydrolase (ARH1)-deficient mice.

open access: yesPLoS ONE, 2018
Cholera toxin, an 84-kDa multimeric protein and a major virulence factor of Vibrio cholerae, uses the ADP-ribosyltransferase activity of its A subunit to intoxicate host cells.
Kizuku Watanabe   +5 more
doaj   +1 more source

Cyclic ADP-Ribose and Hydrogen Peroxide Synergize with ADP-Ribose in the Activation of TRPM2 Channels [PDF]

open access: yesMolecular Cell, 2005
The melastatin-related transient receptor potential channel TRPM2 is a plasma membrane Ca2+-permeable cation channel that is activated by intracellular adenosine diphosphoribose (ADPR) binding to the channel's enzymatic Nudix domain. Channel activity is also seen with nicotinamide dinucleotide (NAD+) and hydrogen peroxide (H2O2), but their mechanisms ...
Kolisek, Martin   +3 more
openaire   +2 more sources

Synthesis of cyclic N1-pentylinosine phosphate, a new structurally reduced cADPR analogue with calcium-mobilizing activity on PC12 cells

open access: yesBeilstein Journal of Organic Chemistry, 2015
Cyclic N1-pentylinosine monophosphate (cpIMP), a novel simplified inosine derivative of cyclic ADP-ribose (cADPR) in which the N1-pentyl chain and the monophosphate group replace the northern ribose and the pyrophosphate moieties, respectively, was ...
Ahmed Mahal   +9 more
doaj   +1 more source

CD38 Structure-Based Inhibitor Design Using the N1-Cyclic Inosine 5'-Diphosphate Ribose Template. [PDF]

open access: yesPLoS ONE, 2013
Few inhibitors exist for CD38, a multifunctional enzyme catalyzing the formation and metabolism of the Ca(2+)-mobilizing second messenger cyclic adenosine 5'-diphosphoribose (cADPR).
Christelle Moreau   +9 more
doaj   +1 more source

Home - About - Disclaimer - Privacy