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Article ; Online: Drug combination therapy for emerging viral diseases.

Shyr, Zeenat A / Cheng, Yu-Shan / Lo, Donald C / Zheng, Wei

2021 Volume 26, Issue 10, Page(s) 2367–2376

Abstract: Effective therapeutics to combat emerging viral infections are an unmet need. Historically, treatments for chronic viral infections with single drugs have not been successful, as exemplified by human immunodeficiency virus (HIV) and hepatitis C virus ( ... ...

Abstract	Effective therapeutics to combat emerging viral infections are an unmet need. Historically, treatments for chronic viral infections with single drugs have not been successful, as exemplified by human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infections. Combination therapy for these diseases has led to improved clinical outcomes with dramatic reductions in viral load, morbidity, and mortality. Drug combinations can enhance therapeutic efficacy through additive, and ideally synergistic, effects for emerging and re-emerging viruses, such as influenza, severe acute respiratory syndrome-coronavirus (SARS-CoV), Middle East respiratory syndrome (MERS)-CoV, Ebola, Zika, and SARS-coronavirus 2 (CoV-2). Although novel drug development through traditional pipelines remains a priority, in the interim, effective synergistic drug candidates could be rapidly identified by drug-repurposing screens, facilitating accelerated paths to clinical testing and potential emergency use authorizations.
MeSH term(s)	Antiviral Agents/therapeutic use ; Communicable Diseases, Emerging/drug therapy ; Drug Combinations ; Drug Repositioning ; Drug Therapy, Combination/trends ; Humans ; Virus Diseases/drug therapy ; COVID-19 Drug Treatment
Chemical Substances	Antiviral Agents ; Drug Combinations
Language	English
Publishing date	2021-05-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2021.05.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes through mitigation of oxidative and ER stress.

Shyr, Zeenat A / Yan, Zihan / Ustione, Alessandro / Egan, Erin M / Remedi, Maria S

PloS one

2022 Volume 17, Issue 2, Page(s) e0258054

Abstract: Progressive loss of pancreatic β-cell functional mass and anti-diabetic drug responsivity are classic findings in diabetes, frequently attributed to compensatory insulin hypersecretion and β-cell exhaustion. However, loss of β-cell mass and identity ... ...

Abstract	Progressive loss of pancreatic β-cell functional mass and anti-diabetic drug responsivity are classic findings in diabetes, frequently attributed to compensatory insulin hypersecretion and β-cell exhaustion. However, loss of β-cell mass and identity still occurs in mouse models of human KATP-gain-of-function induced Neonatal Diabetes Mellitus (NDM), in the absence of insulin secretion. Here we studied the temporal progression and mechanisms underlying glucotoxicity-induced loss of functional β-cell mass in NDM mice, and the effects of sodium-glucose transporter 2 inhibitors (SGLT2i) therapy. Upon tamoxifen induction of transgene expression, NDM mice rapidly developed severe diabetes followed by an unexpected loss of insulin content, decreased proinsulin processing and increased proinsulin at 2-weeks of diabetes. These early events were accompanied by a marked increase in β-cell oxidative and ER stress, without changes in islet cell identity. Strikingly, treatment with the SGLT2 inhibitor dapagliflozin restored insulin content, decreased proinsulin:insulin ratio and reduced oxidative and ER stress. However, despite reduction of blood glucose, dapagliflozin therapy was ineffective in restoring β-cell function in NDM mice when it was initiated at >40 days of diabetes, when loss of β-cell mass and identity had already occurred. Our data from mouse models demonstrate that: i) hyperglycemia per se, and not insulin hypersecretion, drives β-cell failure in diabetes, ii) recovery of β-cell function by SGLT2 inhibitors is potentially through reduction of oxidative and ER stress, iii) SGLT2 inhibitors revert/prevent β-cell failure when used in early stages of diabetes, but not when loss of β-cell mass/identity already occurred, iv) common execution pathways may underlie loss and recovery of β-cell function in different forms of diabetes. These results may have important clinical implications for optimal therapeutic interventions in individuals with diabetes, particularly for those with long-standing diabetes.
MeSH term(s)	Administration, Oral ; Animals ; Benzhydryl Compounds/administration & dosage ; Blood Glucose/metabolism ; Diabetes Mellitus/chemically induced ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Disease Models, Animal ; Endoplasmic Reticulum Stress/drug effects ; Female ; Gain of Function Mutation/drug effects ; Glucosides/administration & dosage ; Humans ; Infant, Newborn ; Infant, Newborn, Diseases/chemically induced ; Infant, Newborn, Diseases/drug therapy ; Infant, Newborn, Diseases/genetics ; Infant, Newborn, Diseases/metabolism ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; KATP Channels/genetics ; Male ; Mice ; Mice, Transgenic ; Oxidative Stress/drug effects ; Protective Agents/administration & dosage ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Sodium-Glucose Transporter 2 Inhibitors/administration & dosage ; Treatment Outcome
Chemical Substances	Benzhydryl Compounds ; Blood Glucose ; Glucosides ; KATP Channels ; Protective Agents ; Sodium-Glucose Transporter 2 Inhibitors ; dapagliflozin (1ULL0QJ8UC)
Language	English
Publishing date	2022-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0258054
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes through mitigation of oxidative and ER stress.

Zeenat A Shyr / Zihan Yan / Alessandro Ustione / Erin M Egan / Maria S Remedi

PLoS ONE, Vol 17, Iss 2, p e

2022 Volume 0258054

Abstract	Progressive loss of pancreatic β-cell functional mass and anti-diabetic drug responsivity are classic findings in diabetes, frequently attributed to compensatory insulin hypersecretion and β-cell exhaustion. However, loss of β-cell mass and identity still occurs in mouse models of human KATP-gain-of-function induced Neonatal Diabetes Mellitus (NDM), in the absence of insulin secretion. Here we studied the temporal progression and mechanisms underlying glucotoxicity-induced loss of functional β-cell mass in NDM mice, and the effects of sodium-glucose transporter 2 inhibitors (SGLT2i) therapy. Upon tamoxifen induction of transgene expression, NDM mice rapidly developed severe diabetes followed by an unexpected loss of insulin content, decreased proinsulin processing and increased proinsulin at 2-weeks of diabetes. These early events were accompanied by a marked increase in β-cell oxidative and ER stress, without changes in islet cell identity. Strikingly, treatment with the SGLT2 inhibitor dapagliflozin restored insulin content, decreased proinsulin:insulin ratio and reduced oxidative and ER stress. However, despite reduction of blood glucose, dapagliflozin therapy was ineffective in restoring β-cell function in NDM mice when it was initiated at >40 days of diabetes, when loss of β-cell mass and identity had already occurred. Our data from mouse models demonstrate that: i) hyperglycemia per se, and not insulin hypersecretion, drives β-cell failure in diabetes, ii) recovery of β-cell function by SGLT2 inhibitors is potentially through reduction of oxidative and ER stress, iii) SGLT2 inhibitors revert/prevent β-cell failure when used in early stages of diabetes, but not when loss of β-cell mass/identity already occurred, iv) common execution pathways may underlie loss and recovery of β-cell function in different forms of diabetes. These results may have important clinical implications for optimal therapeutic interventions in individuals with diabetes, particularly for those with long-standing diabetes.
Keywords	Medicine ; R ; Science ; Q
Subject code	571 ; 500
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes through mitigation of oxidative and ER stress

Zeenat A. Shyr / Zihan Yan / Alessandro Ustione / Erin M. Egan / Maria S. Remedi

PLoS ONE, Vol 17, Iss

2022 Volume 2

Abstract	Progressive loss of pancreatic β-cell functional mass and anti-diabetic drug responsivity are classic findings in diabetes, frequently attributed to compensatory insulin hypersecretion and β-cell exhaustion. However, loss of β-cell mass and identity still occurs in mouse models of human KATP-gain-of-function induced Neonatal Diabetes Mellitus (NDM), in the absence of insulin secretion. Here we studied the temporal progression and mechanisms underlying glucotoxicity-induced loss of functional β-cell mass in NDM mice, and the effects of sodium-glucose transporter 2 inhibitors (SGLT2i) therapy. Upon tamoxifen induction of transgene expression, NDM mice rapidly developed severe diabetes followed by an unexpected loss of insulin content, decreased proinsulin processing and increased proinsulin at 2-weeks of diabetes. These early events were accompanied by a marked increase in β-cell oxidative and ER stress, without changes in islet cell identity. Strikingly, treatment with the SGLT2 inhibitor dapagliflozin restored insulin content, decreased proinsulin:insulin ratio and reduced oxidative and ER stress. However, despite reduction of blood glucose, dapagliflozin therapy was ineffective in restoring β-cell function in NDM mice when it was initiated at >40 days of diabetes, when loss of β-cell mass and identity had already occurred. Our data from mouse models demonstrate that: i) hyperglycemia per se, and not insulin hypersecretion, drives β-cell failure in diabetes, ii) recovery of β-cell function by SGLT2 inhibitors is potentially through reduction of oxidative and ER stress, iii) SGLT2 inhibitors revert/prevent β-cell failure when used in early stages of diabetes, but not when loss of β-cell mass/identity already occurred, iv) common execution pathways may underlie loss and recovery of β-cell function in different forms of diabetes. These results may have important clinical implications for optimal therapeutic interventions in individuals with diabetes, particularly for those with long-standing diabetes.
Keywords	Medicine ; R ; Science ; Q
Subject code	571 ; 500
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Drug Discovery Strategies for SARS-CoV-2.

Shyr, Zeenat A / Gorshkov, Kirill / Chen, Catherine Z / Zheng, Wei

The Journal of pharmacology and experimental therapeutics

2020 Volume 375, Issue 1, Page(s) 127–138

Abstract: Coronavirus disease 2019 (COVID-19) is a novel disease caused by the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 virus that was first detected in December of 2019 in Wuhan, China, and has rapidly spread worldwide. The search for a suitable ...

Abstract	Coronavirus disease 2019 (COVID-19) is a novel disease caused by the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 virus that was first detected in December of 2019 in Wuhan, China, and has rapidly spread worldwide. The search for a suitable vaccine as well as effective therapeutics for the treatment of COVID-19 is underway. Drug repurposing screens provide a useful and effective solution for identifying potential therapeutics against SARS-CoV-2. For example, the experimental drug remdesivir, originally developed for Ebola virus infections, has been approved by the US Food and Drug Administration as an emergency use treatment of COVID-19. However, the efficacy and toxicity of this drug need further improvements. In this review, we discuss recent findings on the pathology of coronaviruses and the drug targets for the treatment of COVID-19. Both SARS-CoV-2-specific inhibitors and broad-spectrum anticoronavirus drugs against SARS-CoV, Middle East respiratory syndrome coronavirus, and SARS-CoV-2 will be valuable additions to the anti-SARS-CoV-2 armament. A multitarget treatment approach with synergistic drug combinations containing different mechanisms of action may be a practical therapeutic strategy for the treatment of severe COVID-19. SIGNIFICANCE STATEMENT: Understanding the biology and pathology of RNA viruses is critical to accomplish the challenging task of developing vaccines and therapeutics against SARS-CoV-2. This review highlights the anti-SARS-CoV-2 drug targets and therapeutic development strategies for COVID-19 treatment.
MeSH term(s)	Antiviral Agents/chemistry ; Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Betacoronavirus/drug effects ; Betacoronavirus/immunology ; Betacoronavirus/physiology ; COVID-19 ; COVID-19 Vaccines ; Clinical Trials as Topic ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/prevention & control ; Drug Discovery/methods ; Humans ; Pandemics/prevention & control ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/prevention & control ; SARS-CoV-2 ; Viral Vaccines/immunology ; Viral Vaccines/therapeutic use ; Virus Internalization/drug effects ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; COVID-19 Vaccines ; Viral Vaccines
Keywords	covid19
Language	English
Publishing date	2020-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.120.000123
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes.

Yan, Zihan / Fortunato, Manuela / Shyr, Zeenat A / Clark, Amy L / Fuess, Matt / Nichols, Colin G / Remedi, Maria S

Diabetes

2022 Volume 71, Issue 6, Page(s) 1233–1245

Abstract: β-Cell failure and loss of β-cell mass are key events in diabetes progression. Although insulin hypersecretion in early stages has been implicated in β-cell exhaustion/failure, loss of β-cell mass still occurs in KATP gain-of-function (GOF) mouse models ... ...

Abstract	β-Cell failure and loss of β-cell mass are key events in diabetes progression. Although insulin hypersecretion in early stages has been implicated in β-cell exhaustion/failure, loss of β-cell mass still occurs in KATP gain-of-function (GOF) mouse models of human neonatal diabetes in the absence of insulin secretion. Thus, we hypothesize that hyperglycemia-induced increased β-cell metabolism is responsible for β-cell failure and that reducing glucose metabolism will prevent loss of β-cell mass. To test this, KATP-GOF mice were crossed with mice carrying β-cell-specific glucokinase haploinsufficiency (GCK+/-), to genetically reduce glucose metabolism. As expected, both KATP-GOF and KATP-GOF/GCK+/- mice showed lack of glucose-stimulated insulin secretion. However, KATP-GOF/GCK+/- mice demonstrated markedly reduced blood glucose, delayed diabetes progression, and improved glucose tolerance compared with KATP-GOF mice. In addition, decreased plasma insulin and content, increased proinsulin, and augmented plasma glucagon observed in KATP-GOF mice were normalized to control levels in KATP-GOF/GCK+/- mice. Strikingly, KATP-GOF/GCK+/- mice demonstrated preserved β-cell mass and identity compared with the marked decrease in β-cell identity and increased dedifferentiation observed in KATP-GOF mice. Moreover KATP-GOF/GCK+/- mice demonstrated restoration of body weight and liver and brown/white adipose tissue mass and function and normalization of physical activity and metabolic efficiency compared with KATP-GOF mice. These results demonstrate that decreasing β-cell glucose signaling can prevent glucotoxicity-induced loss of insulin content and β-cell failure independently of compensatory insulin hypersecretion and β-cell exhaustion.
MeSH term(s)	Animals ; Diabetes Mellitus/metabolism ; Glucokinase/genetics ; Glucokinase/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Mice ; Mice, Transgenic
Chemical Substances	Insulin ; Glucokinase (EC 2.7.1.2) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db21-0992
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Article ; Online: The role of membrane excitability in pancreatic β-cell glucotoxicity.

Shyr, Zeenat A / Wang, Zhiyu / York, Nathaniel W / Nichols, Colin G / Remedi, Maria S

Scientific reports

2019 Volume 9, Issue 1, Page(s) 6952

Abstract: Persistent hyperglycemia is causally associated with pancreatic β-cell dysfunction and loss of pancreatic insulin. Glucose normally enhances β-cell excitability through inhibition of ... ...

Abstract	Persistent hyperglycemia is causally associated with pancreatic β-cell dysfunction and loss of pancreatic insulin. Glucose normally enhances β-cell excitability through inhibition of K
MeSH term(s)	Animals ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cell Membrane/pathology ; Glucose/pharmacology ; Insulin/metabolism ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; KATP Channels/physiology ; Mice ; Mice, Knockout ; Proinsulin/metabolism ; Sweetening Agents/pharmacology
Chemical Substances	Insulin ; KATP Channels ; Sweetening Agents ; Proinsulin (9035-68-1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-05-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-43452-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Drug Discovery Strategies for SARS-CoV-2

Shyr, Zeenat A / Gorshkov, Kirill / Chen, Catherine Z / Zheng, Wei

J Pharmacol Exp Ther

Abstract	Coronavirus disease 2019 (COVID-19) is a novel disease caused by the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 virus that was first detected in December of 2019 in Wuhan, China, and has rapidly spread worldwide. The search for a suitable vaccine as well as effective therapeutics for the treatment of COVID-19 is underway. Drug repurposing screens provide a useful and effective solution for identifying potential therapeutics against SARS-CoV-2. For example, the experimental drug remdesivir, originally developed for Ebola virus infections, has been approved by the US Food and Drug Administration as an emergency use treatment of COVID-19. However, the efficacy and toxicity of this drug need further improvements. In this review, we discuss recent findings on the pathology of coronaviruses and the drug targets for the treatment of COVID-19. Both SARS-CoV-2-specific inhibitors and broad-spectrum anticoronavirus drugs against SARS-CoV, Middle East respiratory syndrome coronavirus, and SARS-CoV-2 will be valuable additions to the anti-SARS-CoV-2 armament. A multitarget treatment approach with synergistic drug combinations containing different mechanisms of action may be a practical therapeutic strategy for the treatment of severe COVID-19. SIGNIFICANCE STATEMENT: Understanding the biology and pathology of RNA viruses is critical to accomplish the challenging task of developing vaccines and therapeutics against SARS-CoV-2. This review highlights the anti-SARS-CoV-2 drug targets and therapeutic development strategies for COVID-19 treatment.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #691116
Database	COVID19

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Article ; Online: The role of membrane excitability in pancreatic β-cell glucotoxicity

Zeenat A. Shyr / Zhiyu Wang / Nathaniel W. York / Colin G. Nichols / Maria S. Remedi

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 12

Abstract: Abstract Persistent hyperglycemia is causally associated with pancreatic β-cell dysfunction and loss of pancreatic insulin. Glucose normally enhances β-cell excitability through inhibition of KATP channels, opening of voltage-dependent calcium channels, ... ...

Abstract	Abstract Persistent hyperglycemia is causally associated with pancreatic β-cell dysfunction and loss of pancreatic insulin. Glucose normally enhances β-cell excitability through inhibition of KATP channels, opening of voltage-dependent calcium channels, increased [Ca2+]i, which triggers insulin secretion. Glucose-dependent excitability is lost in islets from KATP-knockout (KATP-KO) mice, in which β-cells are permanently hyperexcited, [Ca2+]i, is chronically elevated and insulin is constantly secreted. Mouse models of human neonatal diabetes in which KATP gain-of-function mutations are expressed in β-cells (KATP-GOF) also lose the link between glucose metabolism and excitation-induced insulin secretion, but in this case KATP-GOF β-cells are chronically underexcited, with permanently low [Ca2+]i and lack of glucose-dependent insulin secretion. We used KATP-GOF and KATP-KO islets to examine the role of altered-excitability in glucotoxicity. Wild-type islets showed rapid loss of insulin content when chronically incubated in high-glucose, an effect that was reversed by subsequently switching to low glucose media. In contrast, hyperexcitable KATP-KO islets lost insulin content in both low- and high-glucose, while underexcitable KATP-GOF islets maintained insulin content in both conditions. Loss of insulin content in chronic excitability was replicated by pharmacological inhibition of KATP by glibenclamide, The effects of hyperexcitable and underexcitable islets on glucotoxicity observed in in vivo animal models are directly opposite to the effects observed in vitro: we clearly demonstrate here that in vitro, hyperexcitability is detrimental to islets whereas underexcitability is protective.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2019-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High-fat-diet-induced remission of diabetes in a subset of K

Yan, Zihan / Shyr, Zeenat A / Fortunato, Manuela / Welscher, Alecia / Alisio, Mariana / Martino, Michael / Finck, Brian N / Conway, Hannah / Remedi, Maria S

Diabetes, obesity & metabolism

2018 Volume 20, Issue 11, Page(s) 2574–2584

Abstract: Aims: To examine the effects of a high-fat-diet (HFD) on monogenic neonatal diabetes, without the confounding effects of compensatory hyperinsulinaemia.: Methods: Mice expressing K: Results: Surprisingly, K: Conclusion: Together, our results ... ...

Abstract	Aims: To examine the effects of a high-fat-diet (HFD) on monogenic neonatal diabetes, without the confounding effects of compensatory hyperinsulinaemia. Methods: Mice expressing K Results: Surprisingly, K Conclusion: Together, our results suggest that restriction of dietary carbohydrates and caloric replacement by fat can induce metabolic changes that are beneficial in reducing glucotoxicity and secondary consequences of diabetes in a mouse model of insulin-secretory deficiency.
MeSH term(s)	Animals ; Cells, Cultured ; Diabetes Mellitus, Experimental/diet therapy ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diet, High-Fat ; Female ; Gain of Function Mutation ; Gene Knock-In Techniques ; Insulin Resistance/genetics ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Male ; Mice ; Mice, Transgenic ; Obesity/complications ; Obesity/genetics ; Obesity/pathology ; Organ Specificity/genetics ; Potassium Channels, Inwardly Rectifying/genetics ; Remission Induction
Chemical Substances	Kir6.2 channel ; Potassium Channels, Inwardly Rectifying
Language	English
Publishing date	2018-07-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.13423
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