Michael Huang

ORCID: 0000-0003-0693-7833
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Genetic Neurodegenerative Diseases
  • Trace Elements in Health
  • Mechanisms of cancer metastasis
  • Endoplasmic Reticulum Stress and Disease
  • Iron Metabolism and Disorders
  • Metabolism and Genetic Disorders
  • Cancer Mechanisms and Therapy
  • Autophagy in Disease and Therapy
  • Hemoglobinopathies and Related Disorders
  • Drug Transport and Resistance Mechanisms
  • Nanoparticle-Based Drug Delivery
  • Diabetes Treatment and Management
  • Diabetes Management and Research
  • Coenzyme Q10 studies and effects
  • Adenosine and Purinergic Signaling
  • Metal complexes synthesis and properties
  • Protein Interaction Studies and Fluorescence Analysis
  • Melanoma and MAPK Pathways
  • DNA Repair Mechanisms
  • Protein Kinase Regulation and GTPase Signaling
  • Tryptophan and brain disorders
  • Ubiquitin and proteasome pathways
  • Magnesium in Health and Disease
  • Synthesis and bioactivity of alkaloids

Baker Heart and Diabetes Institute
2023-2025

The University of Melbourne
2024

Monash University
2024

Camden and Campbelltown Hospitals
2024

Robert Bosch (Australia)
2013-2023

The University of Sydney
2013-2023

National Health and Medical Research Council
2023

Rice University
2011-2019

Hong Kong Polytechnic University
2017

First Affiliated Hospital of Xi'an Jiaotong University
2016-2017

We used the muscle creatine kinase (MCK) conditional frataxin knockout mouse to elucidate how deficiency alters iron metabolism. This is of significance because leads Friedreich's ataxia, a disease marked by neurologic and cardiologic degeneration. Using cardiac tissues, we demonstrate that down-regulation key molecules involved in 3 mitochondrial utilization pathways: iron-sulfur cluster (ISC) synthesis (iron-sulfur scaffold protein1/2 cysteine desulferase Nfs1), storage (mitochondrial...

10.1073/pnas.0906784106 article EN Proceedings of the National Academy of Sciences 2009-09-05

There is no effective treatment for the cardiomyopathy of most common autosomal recessive ataxia, Friedreich ataxia (FA). This disease due to decreased expression mitochondrial protein, frataxin, which leads alterations in iron (Fe) metabolism. The identification potentially toxic Fe deposits FA suggests plays a role its pathogenesis. Studies using muscle creatine kinase (MCK) conditional frataxin knockout mouse that mirrors have demonstrated deletion alters cardiac Indeed, there are...

10.1073/pnas.1215349109 article EN Proceedings of the National Academy of Sciences 2012-11-20

// Wensheng Liu 1, 2 , Fei Yue 1 Minhua Zheng Angelica Merlot Dong-Hun Bae Michael Huang Darius Lane Patric Jansson Goldie Yuan Lam Vera Richardson Sumit Sahni Danuta Kalinowski Zaklina Kovacevic Des. R. Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School Medicine, 200025, P.R.China Molecular Pharmacology and Pathology Program, Bosch Institute, Blackburn Building (D06), Sydney, New South Wales 2006, Australia Correspondence to: Des Richardson, e-mail:...

10.18632/oncotarget.3316 article EN Oncotarget 2015-04-10

BRCC36-deubiquitinating enzyme (DUB) forms two different complexes through interactions with adaptor proteins Abraxas and ABRO1 in cells. mainly localizes the nucleus, mediating interaction of BRCC36 BRCA1. is localized cytoplasm. Because it lacks BRCA1-interacting motif, complex does not interact Both BRCC36-containing contain common components including BRE NBA1/MERIT40. Here, we found that are assembled a similar manner NBA1 critical for maintaining integrity both complexes. Knockdown or...

10.1074/jbc.m110.200857 article EN cc-by Journal of Biological Chemistry 2011-02-01

The metastasis suppressor, N-myc downstream-regulated gene-1 (NDRG1), plays multifaceted roles in inhibiting oncogenic signaling and can suppress the epithelial mesenchymal transition (EMT), a key step metastasis. In this investigation, NDRG1 inhibited effects of transforming growth factor-β (TGF-β) PANC-1 pancreatic cancer cells, promoting expression co-localization E-cadherin β-catenin at cell membrane. A similar effect supporting membrane was also demonstrated for HT-29 colon CFPAC-1...

10.1093/carcin/bgy178 article EN Carcinogenesis 2018-12-13

Metastasis is a complex process that regulated by multiple signaling pathways, with the focal adhesion kinase (FAK)/paxillin pathway playing major role in formation of adhesions and cell motility. N-myc downstream gene-1 (NDRG1) potent metastasis suppressor many solid tumor types, including prostate colon cancer. Considering antimetastatic effect NDRG1 crucial involvement FAK/paxillin cellular migration cell-matrix adhesion, we assessed effects on this important oncogenic pathway. In present...

10.1124/mol.115.103044 article EN Molecular Pharmacology 2016-02-19

Multidrug resistance (MDR) is a major obstacle in cancer treatment due to the ability of tumor cells efflux chemotherapeutics via drug transporters (e.g. P-glycoprotein (Pgp; ABCB1)). Although mechanism Pgp-mediated known at plasma membrane, functional role intracellular Pgp unclear. Moreover, there has been intense focus on micro-environment as target for treatment. This investigation aimed dissect effects micro-environmental stress subcellular expression, localization, and its MDR. These...

10.1074/jbc.m116.772699 article EN cc-by Journal of Biological Chemistry 2018-01-05

The rise in drug-resistant strains of <i>Mycobacterium tuberculosis</i> is a major threat to human health and highlights the need for new therapeutic strategies. In this study, we have assessed whether high-affinity iron chelators pyridoxal isonicotinoyl hydrazone (PIH) class can restrict growth clinically significant mycobacteria. Screening library PIH derivatives revealed that one compound, namely, 2-pyridylcarboxaldehyde (PCIH), exhibited nanomolar vitro activity against bovis</i> bacille...

10.1124/mol.113.090357 article EN Molecular Pharmacology 2013-11-15
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