Joseph Hinchey

ORCID: 0000-0003-0009-1769
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About
Contact & Profiles
Research Areas
  • Tuberculosis Research and Epidemiology
  • Mycobacterium research and diagnosis
  • Cell Adhesion Molecules Research
  • Autism Spectrum Disorder Research
  • Genetics and Neurodevelopmental Disorders
  • Caveolin-1 and cellular processes
  • Protein Degradation and Inhibitors
  • Toxoplasma gondii Research Studies
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • Immunodeficiency and Autoimmune Disorders
  • Proteoglycans and glycosaminoglycans research
  • interferon and immune responses
  • Erythrocyte Function and Pathophysiology
  • Congenital heart defects research
  • Ubiquitin and proteasome pathways

Albert Einstein College of Medicine
2008-2016

Yeshiva University
2007-2016

Post-translational modification marked by the covalent attachment of ubiquitin-like protein SUMO-1/SMT3C has been implicated in a wide variety cellular processes. Recently, two cDNAs encoding proteins related to SUMO-1 have identified human and mouse. The functions regulation these proteins, known as SUMO-2/SMT3A SUMO-3/SMT3B, remain largely uncharacterized. We describe herein quantitative qualitative distinctions between SUMO-2/3 vertebrate cells. Much this was accomplished through...

10.1074/jbc.275.9.6252 article EN cc-by Journal of Biological Chemistry 2000-03-01

The inhibition of apoptosis infected host cells is a well-known but poorly understood function pathogenic mycobacteria. We show that inactivation the secA2 gene in Mycobacterium tuberculosis, which encodes component virulence-associated protein secretion system, enhanced macrophages by diminishing mycobacterial superoxide dismutase. Deletion markedly increased priming antigen-specific CD8+ T vivo, and vaccination mice guinea pigs with mutant significantly resistance to M. tuberculosis...

10.1172/jci31947 article EN Journal of Clinical Investigation 2007-08-01

Fragile X syndrome (FXS) is the leading cause of both intellectual disability and autism resulting from a single gene mutation. Previously, we characterized cognitive impairments brain structural defects in Drosophila model FXS demonstrated that these were rescued by treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium. A well-documented biochemical defect observed fly mouse models patients low cAMP levels. levels can be regulated mGluR signaling. Herein, demonstrate...

10.1523/jneurosci.1356-12.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-01-07

Fragile X is the most common monogenic disorder associated with intellectual disability (ID) and autism spectrum disorders (ASD). Additionally, many patients are afflicted executive dysfunction, ADHD, seizure sleep disturbances. caused by loss of FMRP expression, which encoded FMR1 gene. Both fly mouse models fragile also based on having no functional protein expression their respective homologs. The model displays well defined cognitive impairments structural brain defects model, although...

10.3389/fnbeh.2016.00136 article EN cc-by Frontiers in Behavioral Neuroscience 2016-06-30

Tuberculosis (TB) caused by Mycobacterium tuberculosis remains a major global health problem, despite the widespread use of M. bovis Bacille Calmette-Guerin (BCG) vaccine and availability drug therapies. In recent years, high incidence coinfection HIV, as well escalating problems associated with resistance, has raised ominous concerns regard to TB control. Vaccination BCG not proven highly effective in controlling TB, also been increasing about potential for cause disseminated mycobacterial...

10.1371/journal.pone.0015857 article EN cc-by PLoS ONE 2011-01-10
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