José R. Godoy

ORCID: 0000-0001-7560-6048
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About
Contact & Profiles
Research Areas
  • Redox biology and oxidative stress
  • Drug Transport and Resistance Mechanisms
  • Connexins and lens biology
  • Glutathione Transferases and Polymorphisms
  • Heat shock proteins research
  • Pharmacological Effects and Toxicity Studies
  • Sulfur Compounds in Biology
  • Metalloenzymes and iron-sulfur proteins
  • Trace Elements in Health
  • Ion Transport and Channel Regulation
  • Metal-Catalyzed Oxygenation Mechanisms
  • S100 Proteins and Annexins
  • Cardiac Ischemia and Reperfusion
  • Organ Transplantation Techniques and Outcomes
  • Anesthesia and Neurotoxicity Research
  • Ethics and bioethics in healthcare
  • Helminth infection and control
  • Nitric Oxide and Endothelin Effects
  • Silk-based biomaterials and applications
  • Bacterial Genetics and Biotechnology
  • Religious and Theological Studies
  • Axon Guidance and Neuronal Signaling
  • Molecular Sensors and Ion Detection
  • Epigenetics and DNA Methylation
  • Amino Acid Enzymes and Metabolism

Long Island University
2020-2022

Ross University School of Veterinary Medicine
2017-2018

University of Veterinary Medicine Vienna
2013-2017

Philipps University of Marburg
2010-2011

Justus-Liebig-Universität Gießen
2004-2008

Institute of Pharmacology
2005

The proteins from the thioredoxin family are crucial actors in redox signaling and cellular response to oxidative stress. major intracellular source for oxygen radicals components of respiratory chain mitochondria. Here, we show that mitochondrial 2-Cys peroxiredoxin (Prx3) is not only substrate 2 (Trx2), but can also be reduced by glutaredoxin (Grx2) via dithiol reaction mechanism. Grx2 reduces Prx3 exhibiting catalytic constants (<i>K<sub>m</sub></i>, 23.8 μmol·liter<sup>−1</sup>;...

10.1074/jbc.m110.185827 article EN cc-by Journal of Biological Chemistry 2010-10-08

Cellular functions and survival are dependent on a tightly controlled redox potential. Currently, an increasing amount of data supports the concept local changes in environment specific signaling events controlling cell function. Specific protein thiol groups major targets regulation. Thioredoxins glutaredoxins catalyze reversible thiol-disulfide exchange reactions primary regulators state. Here, we demonstrate that embryonic brain development depends enzymatic activity glutaredoxin 2....

10.1073/pnas.1110085108 article EN Proceedings of the National Academy of Sciences 2011-12-02

We have cloned human sodium-dependent organic anion transporter (SOAT) cDNA, which consists of 1502 bp and encodes a 377-amino acid protein. SOAT shows 42% sequence identity to the ileal apical bile ASBT 33% hepatic Na(+)/taurocholate-cotransporting polypeptide NTCP. Immunoprecipitation SOAT-FLAG-tagged protein revealed glycosylated form at 46 kDa that decreased 42 after PNGase F treatment. exhibits seven-transmembrane domain topology with an outside-to-inside orientation N-terminal...

10.1074/jbc.m702663200 article EN cc-by Journal of Biological Chemistry 2007-05-10

Glutaredoxin 2 (Grx2) is a glutathione-dependent oxidoreductase involved in the maintenance of mitochondrial redox homeostasis. Grx2 was first characterized as protein, but alternative mRNA variants lacking transit peptide-encoding exon were demonstrated for human and proposed mouse. We systematically screened transcript mouse Grx2. identified total six exons, three constitutive (II, III, IV), two exons (exons Ia Ic), one single-cassette (exon IIIb) located between III IV. Exons Ic IIIb are...

10.1089/ars.2008.2068 article EN Antioxidants and Redox Signaling 2008-09-26

Monothiol glutaredoxins (Grxs) with a noncanonical CGFS active site are found in all kingdoms of life. They include members single domain and thioredoxin-Grx fusion proteins. In Saccharomyces cerevisiae, the multidomain Grx3 Grx4 play an essential role intracellular iron trafficking. This crucial task is mediated by Fe/S cofactor. study shows that this unique physiological cannot be executed Grxs, because thioredoxin indispensable for function vivo. Mutational analysis revealed CPxS motif...

10.1089/ars.2010.3811 article EN Antioxidants and Redox Signaling 2011-02-08

MDR1 (ABCB1) P-glycoprotein exerts a protective function in the blood-brain barrier thereby limiting entry of many drugs and other xenobiotics to central nervous system. A nonsense mutation has been described for Collies related dog breeds which abolishes this is associated with increased susceptibility neurotoxic side effects several including ivermectin, moxidectin loperamide. In order evaluate occurrence frequency nt230 (del4) Germany, we screened 1500 dogs. Frequency homozygous mutated...

10.1111/j.1365-2885.2005.00692.x article EN Journal of Veterinary Pharmacology and Therapeutics 2005-11-15

A subpopulation of dogs the Collie and Australian Shepherd breeds show increased sensitivity to central nervous actions ivermectin, doramectin, loperamide, probably several other drugs. The molecular background for this greater is a nonsense mutation in MDR1 efflux pump, which part functional blood-brain barrier normally limits drug penetration into brain. This report describes rapid PCR-based method detection nt230(del4) using small amount genomic DNA from blood cells. Thereby, homozygous...

10.1111/j.1365-2885.2004.00625.x article EN Journal of Veterinary Pharmacology and Therapeutics 2005-02-01

It is currently controversially discussed whether mesenchymal stem cells (MSC) facilitate cartilage regeneration in vivo by a progenitor- or nonprogenitor-mediated mechanism. Here, we describe potentially novel unbiased cell tracking system based on transgenic donor and corresponding immunocompetent marker-tolerant recipient mouse rat lines inbred genetic backgrounds. Tolerance of recipients was achieved expression an immunologically neutral but physicochemically distinguishable variant the...

10.1172/jci.insight.87322 article EN JCI Insight 2017-10-18

Nucleoredoxin (Nrx) is an oxidoreductase of the thioredoxin family proteins. It was shown to act as a signal transducer in some pathways; however, so far, no comprehensive analysis its regulated substrates and functions available. Here, we used combination two different strategies fill this gap. First, analyzed thiol-redox state proteome SH-SY5Y neuroblastoma cells depleted Nrx compared control using differential thiol-labeling technique quantitative mass spectrometry. 171 proteins were...

10.1155/2018/4829872 article EN cc-by Oxidative Medicine and Cellular Longevity 2018-01-01

10.1016/j.bbrc.2004.02.048 article EN Biochemical and Biophysical Research Communications 2004-02-24

Ischemia-reperfusion injury (IRI) is the leading cause of acute renal failure and a significant contributor to delayed graft function. Animal models are only available resources that mimic complexities IRI-associated damage encountered in vivo. This paper describes an effective mouse model unilateral IRI delivers highly reproducible data. Ischemia induced by occluding right pedicle for 30 min followed reperfusion. In addition surgical procedure, sequential overview expected physiological...

10.3791/62749 article EN Journal of Visualized Experiments 2021-07-15

Abstract Ischemia and reperfusion events, such as myocardial infarction (MI), are reported to induce remote organ damage severely compromising patient outcomes. Tissue survival functional restoration relies on the activation of endogenous redox regulatory systems oxidoreductases thioredoxin (Trx) family. Trxs peroxiredoxins (Prxs) essential for regulation protein thiol groups reduction hydrogen peroxide, respectively. Here, we determined whether experimental MI induces changes in Prxs heart...

10.1007/s00418-020-01939-w article EN cc-by Histochemistry and Cell Biology 2020-11-08

Thioredoxin (Trx) family proteins are key players in redox signaling. Here, we have analyzed glutaredoxin (Grx) 1 and Grx2 age-related macular degeneration (AMD) retinal pigment epithelial (ARPE-19) cells. We hypothesized that these redoxins regulate cellular functions signaling circuits such as cell proliferation, Wnt VEGF release been correlated to the pathophysiology of AMD. ARPE-19 cells were transfected with specific siRNAs silence expression Grx1 for proliferation/viability, migration...

10.1016/j.bbrc.2022.06.030 article EN cc-by Biochemical and Biophysical Research Communications 2022-06-09

Ischemia-reperfusion injury (IRI) is the leading cause of acute renal failure and a significant contributor to delayed graft function. Animal models are only available resources that mimic complexities IRI-associated damage encountered in vivo. This paper describes an effective mouse model unilateral IRI delivers highly reproducible data. Ischemia induced by occluding right pedicle for 30 min followed reperfusion. In addition surgical procedure, sequential overview expected physiological...

10.3791/62749-v article EN Journal of Visualized Experiments 2021-07-15
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