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  1. Article ; Online: CRISPR Editing Takes Aim at Ischemia/Reperfusion Injury.

    Reyes Gaido, Oscar E / Anderson, Mark E

    JAMA cardiology

    2024  Volume 8, Issue 6, Page(s) 522–523

    MeSH term(s) Humans ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Gene Editing ; CRISPR-Cas Systems ; Reperfusion Injury/genetics ; Reperfusion Injury/therapy ; Ischemia
    Language English
    Publishing date 2024-04-07
    Publishing country United States
    Document type Journal Article
    ISSN 2380-6591
    ISSN (online) 2380-6591
    DOI 10.1001/jamacardio.2023.0983
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Genome-wide CRISPR screen reveals genetic modifiers of Ca

    Reyes Gaido, Oscar E / Schole, Kate L / Anderson, Mark E / Luczak, Elizabeth D

    bioRxiv : the preprint server for biology

    2023  

    Abstract: ... ...

    Abstract Ca
    Language English
    Publishing date 2023-01-14
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.13.523980
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Boost US federal funding for international trainees.

    Reyes Gaido, Oscar E / Anderson, Mark E

    Nature

    2021  Volume 594, Issue 7861, Page(s) 26

    MeSH term(s) Financing, Government
    Language English
    Publishing date 2021-03-29
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-021-01469-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dietary cholesterol and apolipoprotein A-I are trafficked in endosomes and lysosomes in the live zebrafish intestine.

    Otis, Jessica P / Shen, Meng-Chieh / Caldwell, Blake A / Reyes Gaido, Oscar E / Farber, Steven A

    American journal of physiology. Gastrointestinal and liver physiology

    2019  Volume 316, Issue 3, Page(s) G350–G365

    Abstract: Difficulty in imaging the vertebrate intestine in vivo has hindered our ability to model nutrient and protein trafficking from both the lumenal and basolateral aspects of enterocytes. Our goal was to use live confocal imaging to increase understanding of ...

    Abstract Difficulty in imaging the vertebrate intestine in vivo has hindered our ability to model nutrient and protein trafficking from both the lumenal and basolateral aspects of enterocytes. Our goal was to use live confocal imaging to increase understanding of intestinal trafficking of dietary cholesterol and apolipoprotein A-I (APOA-I), the main structural component of high-density lipoproteins. We developed a novel assay to visualize live dietary cholesterol trafficking in the zebrafish intestine by feeding TopFluor-cholesterol (TF-cholesterol), a fluorescent cholesterol analog, in a lipid-rich, chicken egg yolk feed. Quantitative microscopy of transgenic zebrafish expressing fluorescently tagged protein markers of early, recycling, and late endosomes/lysosomes provided the first evidence, to our knowledge, of cholesterol transport in the intestinal endosomal-lysosomal trafficking system. To study APOA-I dynamics, transgenic zebrafish expressing an APOA-I fluorescent fusion protein (APOA-I-mCherry) from tissue-specific promoters were created. These zebrafish demonstrated that APOA-I-mCherry derived from the intestine accumulated in the liver and vice versa. Additionally, intracellular APOA-I-mCherry localized to endosomes and lysosomes in the intestine and liver. Moreover, live imaging demonstrated that APOA-I-mCherry colocalized with dietary TF-cholesterol in enterocytes, and this colocalization increased with feeding time. This study provides a new set of tools for the study of cellular lipid biology and elucidates a key role for endosomal-lysosomal trafficking of intestinal cholesterol and APOA-I. NEW & NOTEWORTHY A fluorescent cholesterol analog was fed to live, translucent larval zebrafish to visualize intracellular cholesterol and apolipoprotein A-I (APOA-I) trafficking. With this model intestinal endosomal-lysosomal cholesterol trafficking was observed for the first time. A new APOA-I fusion protein (APOA-I-mCherry) expressed from tissue-specific promoters was secreted into the circulation and revealed that liver-derived APOA-I-mCherry accumulates in the intestine and vice versa. Intestinal, intracellular APOA-I-mCherry was observed in endosomes and lysosomes and colocalized with dietary cholesterol.
    MeSH term(s) Animals ; Apolipoprotein A-I/adverse effects ; Biological Transport/physiology ; Cholesterol/metabolism ; Cholesterol, Dietary/metabolism ; Endosomes/metabolism ; Enterocytes/metabolism ; Intestines/physiology ; Lipoproteins, HDL/metabolism ; Lysosomes/metabolism ; Protein Transport/physiology ; Zebrafish
    Chemical Substances Apolipoprotein A-I ; Cholesterol, Dietary ; Lipoproteins, HDL ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2019-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00080.2018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: CaMKII as a Therapeutic Target in Cardiovascular Disease.

    Reyes Gaido, Oscar E / Nkashama, Lubika J / Schole, Kate L / Wang, Qinchuan / Umapathi, Priya / Mesubi, Olurotimi O / Konstantinidis, Klitos / Luczak, Elizabeth D / Anderson, Mark E

    Annual review of pharmacology and toxicology

    2022  Volume 63, Page(s) 249–272

    Abstract: CaMKII (the multifunctional ... ...

    Abstract CaMKII (the multifunctional Ca
    MeSH term(s) Humans ; Cardiovascular Diseases/drug therapy ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Arrhythmias, Cardiac ; Cardiovascular System/metabolism ; Signal Transduction/physiology
    Chemical Substances Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)
    Language English
    Publishing date 2022-08-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 196587-6
    ISSN 1545-4304 ; 0362-1642
    ISSN (online) 1545-4304
    ISSN 0362-1642
    DOI 10.1146/annurev-pharmtox-051421-111814
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor.

    Reyes Gaido, Oscar E / Pavlaki, Nikoleta / Granger, Jonathan M / Mesubi, Olurotimi O / Liu, Bian / Lin, Brian L / Long, Alan / Walker, David / Mayourian, Joshua / Schole, Kate L / Terrillion, Chantelle E / Nkashama, Lubika J / Hulsurkar, Mohit M / Dorn, Lauren E / Ferrero, Kimberly M / Huganir, Richard L / Müller, Frank U / Wehrens, Xander H T / Liu, Jun O /
    Luczak, Elizabeth D / Bezzerides, Vassilios J / Anderson, Mark E

    Science translational medicine

    2023  Volume 15, Issue 701, Page(s) eabq7839

    Abstract: ... ...

    Abstract Ca
    MeSH term(s) Animals ; Child ; Humans ; Mice ; Arrhythmias, Cardiac ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & inhibitors ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Heart Diseases/metabolism ; Myocytes, Cardiac/metabolism ; Pyrazoles/pharmacology
    Chemical Substances Calcium (SY7Q814VUP) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Pyrazoles ; ruxolitinib (82S8X8XX8H)
    Language English
    Publishing date 2023-06-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abq7839
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Excessive

    Umapathi, Priya / Mesubi, Olurotimi O / Banerjee, Partha S / Abrol, Neha / Wang, Qinchuan / Luczak, Elizabeth D / Wu, Yuejin / Granger, Jonathan M / Wei, An-Chi / Reyes Gaido, Oscar E / Florea, Liliana / Talbot, C Conover / Hart, Gerald W / Zachara, Natasha E / Anderson, Mark E

    Circulation

    2021  Volume 143, Issue 17, Page(s) 1687–1703

    Abstract: Background: Heart failure is a leading cause of death worldwide and is associated with the rising prevalence of obesity, hypertension, and diabetes. : Methods: We developed 2 new transgenic mouse models with myocardial overexpression of OGT and OGA ... ...

    Abstract Background: Heart failure is a leading cause of death worldwide and is associated with the rising prevalence of obesity, hypertension, and diabetes.
    Methods: We developed 2 new transgenic mouse models with myocardial overexpression of OGT and OGA to control
    Results: We found that OGT transgenic hearts showed increased
    Conclusions: Our data provide evidence that excessive
    MeSH term(s) Animals ; Death, Sudden/pathology ; Disease Models, Animal ; Heart Failure/physiopathology ; Humans ; Mice ; Mice, Transgenic ; N-Acetylglucosaminyltransferases/adverse effects
    Chemical Substances N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; O-GlcNAc transferase (EC 2.4.1.-)
    Language English
    Publishing date 2021-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.051911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.

    Luczak, Elizabeth D / Wu, Yuejin / Granger, Jonathan M / Joiner, Mei-Ling A / Wilson, Nicholas R / Gupta, Ashish / Umapathi, Priya / Murphy, Kevin R / Reyes Gaido, Oscar E / Sabet, Amin / Corradini, Eleonora / Tseng, Wen-Wei / Wang, Yibin / Heck, Albert J R / Wei, An-Chi / Weiss, Robert G / Anderson, Mark E

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 4416

    Abstract: Despite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. Here, we report increased ... ...

    Abstract Despite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. Here, we report increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. By contrast, mice with genetic mitochondrial CaMKII inhibition are protected from left ventricular dilation and dysfunction after MI. Mice with myocardial and mitochondrial CaMKII overexpression (mtCaMKII) have severe dilated cardiomyopathy and decreased ATP that causes elevated cytoplasmic resting (diastolic) Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium-Binding Proteins/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cardiomyopathy, Dilated/metabolism ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Heart Failure/metabolism ; Heart Ventricles/physiopathology ; Mice ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Myocardial Infarction/physiopathology ; Myocardial Infarction/surgery ; Signal Transduction
    Chemical Substances Calcium-Binding Proteins ; Mitochondrial Proteins ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-09-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-18165-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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