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Article ; Online: Implications of the NADase CD38 in COVID pathophysiology.

Zeidler, Julianna D / Kashyap, Sonu / Hogan, Kelly A / Chini, Eduardo Nunes

2021 Volume 102, Issue 1, Page(s) 339–341

Abstract: During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such ...

Abstract	During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such as mass immunization, most experimental or repurposed drugs have failed in large randomized clinical trials (https://www.who.int/publications/i/item/therapeutics-and-covid-19-living-guideline). The worldwide spread of SARS-CoV-2 virus revealed specific susceptibilities to the virus among the elderly and individuals with age-related syndromes. These populations were more likely to experience a hyperimmune response characterized by a treatment-resistant acute lung pathology accompanied by multiple organ failure. These observations underscore the interplay between the virus, the biology of aging, and outcomes observed in the most severe cases of SARS-CoV-2 infection. The ectoenzyme CD38 has been implicated in the process of "inflammaging" in aged tissues. In a current publication, Horenstein et al. present evidence to support the hypothesis that CD38 plays a central role in altered immunometabolism resulting from COVID-19 infection. The authors discuss a critical but underappreciated trifecta of CD38-mediated NAD
MeSH term(s)	ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; Aging ; COVID-19/physiopathology ; Gene Expression Regulation, Enzymologic ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; NAD/metabolism ; SARS-CoV-2
Chemical Substances	Membrane Glycoproteins ; NAD (0U46U6E8UK) ; CD38 protein, human (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2021-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00007.2021
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Article: Using mass spectrometry imaging to visualize age-related subcellular disruption.

Hogan, Kelly A / Zeidler, Julianna D / Beasley, Heather K / Alsaadi, Abrar I / Alshaheeb, Abdulkareem A / Chang, Yi-Chin / Tian, Hua / Hinton, Antentor O / McReynolds, Melanie R

Frontiers in molecular biosciences

2023 Volume 10, Page(s) 906606

Abstract: Metabolic homeostasis balances the production and consumption of energetic molecules to maintain active, healthy cells. Cellular stress, which disrupts metabolism and leads to the loss of cellular homeostasis, is important in age-related diseases. We ... ...

Abstract	Metabolic homeostasis balances the production and consumption of energetic molecules to maintain active, healthy cells. Cellular stress, which disrupts metabolism and leads to the loss of cellular homeostasis, is important in age-related diseases. We focus here on the role of organelle dysfunction in age-related diseases, including the roles of energy deficiencies, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, changes in metabolic flux in aging (e.g., Ca
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2023.906606
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Article ; Online: Implications of the PAPP-A-IGFBP-IGF-1 pathway in the pathogenesis and treatment of polycystic kidney disease.

Kashyap, Sonu / Zeidler, Julianna D / Chini, Claudia C S / Chini, Eduardo Nunes

Cellular signalling

2020 Volume 73, Page(s) 109698

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases implicated in the development of end stage renal disease (ESRD). Although FDA has recently approved a drug against ADPKD, there is still a great need for ... ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases implicated in the development of end stage renal disease (ESRD). Although FDA has recently approved a drug against ADPKD, there is still a great need for development of alternative management strategies for ADPKD. Understanding the different mechanisms that lead to cystogenesis and cyst expansion in ADPKD is imperative to develop new therapies against ADPKD. Recently, we demonstrated that caloric restriction can prevent the development of cystic disease in animal models of ADPKD and through these studies identified a new role for pregnancy associated plasma protein-A (PAPP-A), a component of the insulin-like growth factors (IGF) pathway, in the pathogenesis of this disease. The PAPP-A-IGF pathway plays an important role in regulation of cell growth, differentiation, and transformation and dysregulation of this pathway has been implicated in many diseases. Several indirect studies support the involvement of IGF-1 in the pathogenesis of ADPKD. However, it was only recently that we described a direct role for a component of this pathway in pathogenesis of ADPKD, opening a new avenue for the therapeutic approaches for this cystic disease. The present literature review will critically discuss the evidence that supports the role of components of IGF pathway in the pathogenesis of ADPKD and discuss the pharmacological implications of PAPP-A-IGF axis in this disease.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Humans ; Insulin-Like Growth Factor Binding Proteins/metabolism ; Insulin-Like Growth Factor I/metabolism ; Polycystic Kidney, Autosomal Dominant/metabolism ; Polycystic Kidney, Autosomal Dominant/pathology ; Pregnancy-Associated Plasma Protein-A/physiology
Chemical Substances	IGF1 protein, human ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I (67763-96-6) ; Pregnancy-Associated Plasma Protein-A (EC 3.4.24.-) ; PAPPA protein, human (EC 3.4.24.79)
Language	English
Publishing date	2020-06-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2020.109698
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Article ; Online: Evolving concepts in NAD

Chini, Claudia C S / Zeidler, Julianna D / Kashyap, Sonu / Warner, Gina / Chini, Eduardo Nunes

Cell metabolism

2021 Volume 33, Issue 6, Page(s) 1076–1087

Abstract: NAD(H) and NADP(H) have traditionally been viewed as co-factors (or co-enzymes) involved in a myriad of oxidation-reduction reactions including the electron transport in the mitochondria. However, NAD pathway metabolites have many other important ... ...

Abstract	NAD(H) and NADP(H) have traditionally been viewed as co-factors (or co-enzymes) involved in a myriad of oxidation-reduction reactions including the electron transport in the mitochondria. However, NAD pathway metabolites have many other important functions, including roles in signaling pathways, post-translational modifications, epigenetic changes, and regulation of RNA stability and function via NAD-capping of RNA. Non-oxidative reactions ultimately lead to the net catabolism of these nucleotides, indicating that NAD metabolism is an extremely dynamic process. In fact, recent studies have clearly demonstrated that NAD has a half-life in the order of minutes in some tissues. Several evolving concepts on the metabolism, transport, and roles of these NAD pathway metabolites in disease states such as cancer, neurodegeneration, and aging have emerged in just the last few years. In this perspective, we discuss key recent discoveries and changing concepts in NAD metabolism and biology that are reshaping the field. In addition, we will pose some open questions in NAD biology, including why NAD metabolism is so fast and dynamic in some tissues, how NAD and its precursors are transported to cells and organelles, and how NAD metabolism is integrated with inflammation and senescence. Resolving these questions will lead to significant advancements in the field.
MeSH term(s)	Animals ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; NAD/metabolism ; NADP/metabolism
Chemical Substances	NAD (0U46U6E8UK) ; NADP (53-59-8)
Language	English
Publishing date	2021-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.04.003
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Article ; Online: Ecto-CD38-NADase inhibition modulates cardiac metabolism and protects mice against doxorubicin-induced cardiotoxicity.

Peclat, Thais R / Agorrody, Guillermo / Colman, Laura / Kashyap, Sonu / Zeidler, Julianna D / Chini, Claudia C S / Warner, Gina M / Thompson, Katie L / Dalvi, Pranjali / Beckedorff, Felipe / Ebtehaj, Sanam / Herrmann, Joerg / van Schooten, Wim / Chini, Eduardo Nunes

Cardiovascular research

2024 Volume 120, Issue 3, Page(s) 286–300

Abstract: Aims: Doxorubicin (DXR) is a chemotherapeutic agent that causes dose-dependent cardiotoxicity. Recently, it has been proposed that the NADase CD38 may play a role in doxorubicin-induced cardiotoxicity (DIC). CD38 is the main NAD+-catabolizing enzyme in ... ...

Abstract	Aims: Doxorubicin (DXR) is a chemotherapeutic agent that causes dose-dependent cardiotoxicity. Recently, it has been proposed that the NADase CD38 may play a role in doxorubicin-induced cardiotoxicity (DIC). CD38 is the main NAD+-catabolizing enzyme in mammalian tissues. Interestingly, in the heart, CD38 is mostly expressed as an ecto-enzyme that can be targeted by specific inhibitory antibodies. The goal of the present study is to characterize the role of CD38 ecto-enzymatic activity in cardiac metabolism and the development of DIC. Methods and results: Using both a transgenic animal model and a non-cytotoxic enzymatic anti-CD38 antibody, we investigated the role of CD38 and its ecto-NADase activity in DIC in pre-clinical models. First, we observed that DIC was prevented in the CD38 catalytically inactive (CD38-CI) transgenic mice. Both left ventricular systolic function and exercise capacity were decreased in wild-type but not in CD38-CI mice treated with DXR. Second, blocking CD38-NADase activity with the specific antibody 68 (Ab68) likewise protected mice against DIC and decreased DXR-related mortality by 50%. A reduction of DXR-induced mitochondrial dysfunction, energy deficiency, and inflammation gene expression were identified as the main mechanisms mediating the protective effects. Conclusion: NAD+-preserving strategies by inactivation of CD38 via a genetic or a pharmacological-based approach improve cardiac energetics and reduce cardiac inflammation and dysfunction otherwise seen in an acute DXR cardiotoxicity model.
MeSH term(s)	Mice ; Animals ; NAD+ Nucleosidase/metabolism ; ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; NAD/metabolism ; Cardiotoxicity ; Mice, Transgenic ; Doxorubicin/toxicity ; Inflammation ; Mammals/metabolism
Chemical Substances	NAD+ Nucleosidase (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6) ; NAD (0U46U6E8UK) ; Doxorubicin (80168379AG)
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvae025
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Article ; Online: Using mass spectrometry imaging to visualize age-related subcellular disruption

Kelly A. Hogan / Julianna D. Zeidler / Heather K. Beasley / Abrar I. Alsaadi / Abdulkareem A. Alshaheeb / Yi-Chin Chang / Hua Tian / Antentor O. Hinton / Melanie R. McReynolds

Frontiers in Molecular Biosciences, Vol

2023 Volume 10

Abstract	Metabolic homeostasis balances the production and consumption of energetic molecules to maintain active, healthy cells. Cellular stress, which disrupts metabolism and leads to the loss of cellular homeostasis, is important in age-related diseases. We focus here on the role of organelle dysfunction in age-related diseases, including the roles of energy deficiencies, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, changes in metabolic flux in aging (e.g., Ca2+ and nicotinamide adenine dinucleotide), and alterations in the endoplasmic reticulum-mitochondria contact sites that regulate the trafficking of metabolites. Tools for single-cell resolution of metabolite pools and metabolic flux in animal models of aging and age-related diseases are urgently needed. High-resolution mass spectrometry imaging (MSI) provides a revolutionary approach for capturing the metabolic states of individual cells and cellular interactions without the dissociation of tissues. mass spectrometry imaging can be a powerful tool to elucidate the role of stress-induced cellular dysfunction in aging.
Keywords	mass spec imaging ; MERCs ; Golgi complex ; mitocchondrial dysfunction ; aging ; metabolic flux ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Dihydronicotinamide Riboside Is a Potent NAD

Chini, Claudia C S / Peclat, Thais R / Gomez, Lilian S / Zeidler, Julianna D / Warner, Gina M / Kashyap, Sonu / Mazdeh, Delaram Z / Hayat, Faisal / Migaud, Marie E / Paulus, Aneel / Chanan-Khan, Asher A / Chini, Eduardo N

Frontiers in immunology

2022 Volume 13, Page(s) 840246

Abstract: Nicotinamide adenine dinucleotide (NAD) metabolism plays an important role in the regulation of immune function. However, a complete picture of how NAD, its metabolites, precursors, and metabolizing enzymes work together in regulating immune function and ...

Abstract	Nicotinamide adenine dinucleotide (NAD) metabolism plays an important role in the regulation of immune function. However, a complete picture of how NAD, its metabolites, precursors, and metabolizing enzymes work together in regulating immune function and inflammatory diseases is still not fully understood. Surprisingly, few studies have compared the effect of different forms of vitamin B3 on cellular functions. Therefore, we investigated the role of NAD boosting in the regulation of macrophage activation and function using different NAD precursors supplementation. We compared nicotinamide mononucleotide (NMN), nicotinamide riboside (NR), and nicotinamide (NAM) supplementation, with the recently described potent NAD precursor NRH. Our results show that only NRH supplementation strongly increased NAD
MeSH term(s)	Cytokines ; Glycosides ; Macrophages/metabolism ; NAD/metabolism ; Niacinamide/analogs & derivatives ; Niacinamide/pharmacology ; Phenotype
Chemical Substances	Cytokines ; Glycosides ; dihydronicotinamide ; NAD (0U46U6E8UK) ; Niacinamide (25X51I8RD4)
Language	English
Publishing date	2022-02-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.840246
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Article ; Online: Correction: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus.

Cararo-Lopes, Eduardo / Dias, Matheus H / da Silva, Marcelo S / Zeidler, Julianna D / Vessoni, Alexandre T / Reis, Marcelo S / Boccardo, Enrique / Armelin, Hugo A

Cell death & disease

2021 Volume 12, Issue 4, Page(s) 293

Language	English
Publishing date	2021-03-17
Publishing country	England
Document type	Published Erratum
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-03564-4
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Article ; Online: Mitotherapy prevents peripheral neuropathy induced by oxaliplatin in mice.

Maia, João R L C B / Machado, Loreena K A / Fernandes, Gabriel G / Vitorino, Louise C / Antônio, Letícia S / Araújo, Suzana Maria B / Colodeti, Lilian C / Fontes-Dantas, Fabrícia L / Zeidler, Julianna D / Saraiva, Georgia N / Da Poian, Andrea T / Figueiredo, Claudia P / Passos, Giselle F / da Costa, Robson

Neuropharmacology

2023 Volume 245, Page(s) 109828

Abstract: Oxaliplatin (OXA) is an antineoplastic agent used for the treatment of cisplatin-resistant tumours, presenting lower incidence of nephrotoxicity and myelotoxicity than other platinum-based drugs. However, OXA treatment is highly associated with painful ... ...

Abstract	Oxaliplatin (OXA) is an antineoplastic agent used for the treatment of cisplatin-resistant tumours, presenting lower incidence of nephrotoxicity and myelotoxicity than other platinum-based drugs. However, OXA treatment is highly associated with painful peripheral neuropathy, a well-known and relevant side effect caused by mitochondrial dysfunction. The transfer of functional exogenous mitochondria (mitotherapy) is a promising therapeutic strategy for mitochondrial diseases. We investigated the effect of mitotherapy on oxaliplatin-induced painful peripheral neuropathy (OIPN) in male mice. OIPN was induced by i.p. injections of oxaliplatin (3 mg/kg) over 5 consecutive days. Mechanical (von Frey test) and cold (acetone drop test) allodynia were evaluated between 7 and 17 days after the first OXA treatment. Mitochondria was isolated from donor mouse livers and mitochondrial oxidative phosphorylation was assessed with high resolution respirometry. After confirming that the isolated mitochondria were functional, the organelles were administered at the dose of 0.5 mg/kg of mitochondrial protein on days 1, 3 and 5. Treatment with OXA caused both mechanical and cold allodynia in mice that were significant 7 days after the initial injection of OXA and persisted for up to 17 days. Mitotherapy significantly prevented the development of both sensory alterations, and attenuated body weight loss induced by OXA. Mitotherapy also prevented spinal cord ERK1/2 activation, microgliosis and the increase in TLR4 mRNA levels. Mitotherapy prevented OIPN by inhibiting neuroinflammation and the consequent cellular overactivity in the spinal cord, presenting a potential therapeutic strategy for pain management in oncologic patients undergoing OXA treatment.
MeSH term(s)	Humans ; Male ; Mice ; Animals ; Oxaliplatin/toxicity ; Hyperalgesia/chemically induced ; Hyperalgesia/prevention & control ; Hyperalgesia/drug therapy ; Peripheral Nervous System Diseases/chemically induced ; Peripheral Nervous System Diseases/prevention & control ; Antineoplastic Agents/toxicity ; Pain
Chemical Substances	Oxaliplatin (04ZR38536J) ; Antineoplastic Agents
Language	English
Publishing date	2023-12-27
Publishing country	England
Document type	Journal Article
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2023.109828
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Article ; Online: The CD38 glycohydrolase and the NAD sink: implications for pathological conditions.

Zeidler, Julianna D / Hogan, Kelly A / Agorrody, Guillermo / Peclat, Thais R / Kashyap, Sonu / Kanamori, Karina S / Gomez, Lilian Sales / Mazdeh, Delaram Z / Warner, Gina M / Thompson, Katie L / Chini, Claudia C S / Chini, Eduardo Nunes

American journal of physiology. Cell physiology

2022 Volume 322, Issue 3, Page(s) C521–C545

Abstract: Nicotinamide adenine dinucleotide (NAD) acts as a cofactor in several oxidation-reduction (redox) reactions and is a substrate for a number of nonredox enzymes. NAD is fundamental to a variety of cellular processes including energy metabolism, cell ... ...

Abstract	Nicotinamide adenine dinucleotide (NAD) acts as a cofactor in several oxidation-reduction (redox) reactions and is a substrate for a number of nonredox enzymes. NAD is fundamental to a variety of cellular processes including energy metabolism, cell signaling, and epigenetics. NAD homeostasis appears to be of paramount importance to health span and longevity, and its dysregulation is associated with multiple diseases. NAD metabolism is dynamic and maintained by synthesis and degradation. The enzyme CD38, one of the main NAD-consuming enzymes, is a key component of NAD homeostasis. The majority of CD38 is localized in the plasma membrane with its catalytic domain facing the extracellular environment, likely for the purpose of controlling systemic levels of NAD. Several cell types express CD38, but its expression predominates on endothelial cells and immune cells capable of infiltrating organs and tissues. Here we review potential roles of CD38 in health and disease and postulate ways in which CD38 dysregulation causes changes in NAD homeostasis and contributes to the pathophysiology of multiple conditions. Indeed, in animal models the development of infectious diseases, autoimmune disorders, fibrosis, metabolic diseases, and age-associated diseases including cancer, heart disease, and neurodegeneration are associated with altered CD38 enzymatic activity. Many of these conditions are modified in CD38-deficient mice or by blocking CD38 NADase activity. In diseases in which CD38 appears to play a role, CD38-dependent NAD decline is often a common denominator of pathophysiology. Thus, understanding dysregulation of NAD homeostasis by CD38 may open new avenues for the treatment of human diseases.
MeSH term(s)	ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; Animals ; Endothelial Cells/metabolism ; Glycoside Hydrolases ; Mice ; NAD/metabolism ; NAD+ Nucleosidase/metabolism
Chemical Substances	NAD (0U46U6E8UK) ; Glycoside Hydrolases (EC 3.2.1.-) ; NAD+ Nucleosidase (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00451.2021
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