Deepak Chhangani

Deepak Chhangani, PhD

Assistant Scientist

Department: MD-BEHAVIORAL NEUROLOGY
Business Phone: (352) 273-9192

About Deepak Chhangani

Deepak Chhangani is graduated from Indian Institute of Technology Jodhpur, Rajasthan, INDIA with a PhD degree in Biology. He has specifically worked on Protein Quality Control Mechanisms, its components and their impact on various neurodegenerative conditions including Huntington’s disease (HD), Spinocerebellar Ataxia (SCA) and Amyotrophic lateral sclerosis (ALS). He is currently investigating a common pathological hallmark of ALS and Alzheimer’s disease (AD), known as TDP-43 proteinopathies.

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Research Profile

My major research project involve investigating the role of TDP-43 in Amyotrophic lateral sclerosis (ALS) using Drosophila as a model. Previously, I have completed my PhD from Indian Institute of Technology Jodhpur (IITJ), Rajasthan, INDIA in the field of Molecular Neurobiology. I have studied the role of Protein Quality Control E3 ubiquitin ligases in neurodegeneration during my PhD. I am currently interested in finding the common mechanisms in various TDP-43 proteinopathies including ALS, Frontotemporal lobar degeneration (FTLD) and Alzheimer’s disease (AD).

Open Researcher and Contributor ID (ORCID)

0000-0003-3971-7589

Areas of Interest
  • Alzheimer’s Disease
  • Amyotrophic Lateral Sclerosis
  • Drosophila Genetics
  • Neurobiology of age-related diseases
  • TDP-43 proteinopathies

Publications

2024
Infection and chronic disease activate a systemic brain-muscle signaling axis.
Science immunology. 9(97) [DOI] 10.1126/sciimmunol.adm7908. [PMID] 38996009.
2023
Amyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity.
Molecular neurodegeneration. 18(1) [DOI] 10.1186/s13024-023-00654-z. [PMID] 37710351.
2023
Identification of potential pathways and biomarkers linked to progression in ALS.
Annals of clinical and translational neurology. 10(2):150-165 [DOI] 10.1002/acn3.51697. [PMID] 36533811.
2022
Infection and chronic disease activate a brain-muscle signaling axis that regulates muscle performance.
bioRxiv : the preprint server for biology. [DOI] 10.1101/2020.12.20.423533. [PMID] 33398283.
2022
Nuclear import receptors are recruited by FG-nucleoporins to rescue hallmarks of TDP-43 proteinopathy.
Molecular neurodegeneration. 17(1) [DOI] 10.1186/s13024-022-00585-1. [PMID] 36482422.
2022
TDP-35, a truncated fragment of TDP-43, induces dose-dependent toxicity and apoptosis in flies.
Neural regeneration research. 17(11):2441-2442 [DOI] 10.4103/1673-5374.338997. [PMID] 35535891.
2021
Molecular, functional, and pathological aspects of TDP-43 fragmentation.
iScience. 24(5) [DOI] 10.1016/j.isci.2021.102459. [PMID] 34013172.
2020
Nuclear transport genes as modifiers of TDP-43 toxicity in flies
The Journal of Prevention of Alzheimer's Disease. 1-2 [DOI] 10.14283/jpad.2020.42.
2018
Gp78 involvement in cellular proliferation: Can act as a promising modulator for cell cycle regulatory proteins?
Journal of cellular physiology. 233(10):6352-6368 [DOI] 10.1002/jcp.26618. [PMID] 29741771.
2017
Proteasomal Dysfunction Induced By Diclofenac Engenders Apoptosis Through Mitochondrial Pathway.
Journal of cellular biochemistry. 118(5):1014-1027 [DOI] 10.1002/jcb.25666. [PMID] 27487200.
2017
secHsp70 as a tool to approach amyloid-β42 and other extracellular amyloids.
Fly. 11(3):179-184 [DOI] 10.1080/19336934.2017.1291104. [PMID] 28165856.
2016
Ibuprofen Induces Mitochondrial-Mediated Apoptosis Through Proteasomal Dysfunction.
Molecular neurobiology. 53(10):6968-6981 [PMID] 26666667.
2016
Mahogunin ring finger 1 confers cytoprotection against mutant SOD1 aggresomes and is defective in an ALS mouse model.
Neurobiology of disease. 86:16-28 [DOI] 10.1016/j.nbd.2015.11.017. [PMID] 26607786.
2016
Mahogunin Ring Finger-1 (MGRN1), a Multifaceted Ubiquitin Ligase: Recent Unraveling of Neurobiological Mechanisms.
Molecular neurobiology. 53(7):4484-96 [DOI] 10.1007/s12035-015-9379-8. [PMID] 26255182.
2015
Selective multifaceted E3 ubiquitin ligases barricade extreme defense: Potential therapeutic targets for neurodegeneration and ageing.
Ageing research reviews. 24(Pt B):138-59 [DOI] 10.1016/j.arr.2015.07.009. [PMID] 26247845.
2014
Autophagy coupling interplay: can improve cellular repair and aging?
Molecular neurobiology. 49(3):1270-81 [DOI] 10.1007/s12035-013-8599-z. [PMID] 24385255.
2014
Mahogunin ring finger 1 suppresses misfolded polyglutamine aggregation and cytotoxicity.
Biochimica et biophysica acta. 1842(9):1472-84 [DOI] 10.1016/j.bbadis.2014.04.014. [PMID] 24769000.
2014
Ubiquitin ligase ITCH recruitment suppresses the aggregation and cellular toxicity of cytoplasmic misfolded proteins.
Scientific reports. 4 [DOI] 10.1038/srep05077. [PMID] 24865853.
2013
E6-AP association promotes SOD1 aggresomes degradation and suppresses toxicity.
Neurobiology of aging. 34(4):1310.e11-23 [DOI] 10.1016/j.neurobiolaging.2012.08.016. [PMID] 23040663.
2013
Mahogunin ring finger-1 (MGRN1) suppresses chaperone-associated misfolded protein aggregation and toxicity.
Scientific reports. 3 [DOI] 10.1038/srep01972. [PMID] 23756845.
2013
Misfolded proteins recognition strategies of E3 ubiquitin ligases and neurodegenerative diseases.
Molecular neurobiology. 47(1):302-12 [DOI] 10.1007/s12035-012-8351-0. [PMID] 23001884.
2013
Protein quality control system in neurodegeneration: a healing company hard to beat but failure is fatal.
Molecular neurobiology. 48(1):141-56 [DOI] 10.1007/s12035-013-8411-0. [PMID] 23378031.
2012
E3 ubiquitin ligases in protein quality control mechanism.
Molecular neurobiology. 45(3):571-85 [DOI] 10.1007/s12035-012-8273-x. [PMID] 22610945.

Education

PhD in Biology
2016 · Indian Institute of Technology Jodhpur, Rajasthan, INDIA
M.Sc. in Biotechnology
2008 · MN College, Bikaner, Rajasthan, INDIA
B.Sc. in Chemisty, Botany and Zoology
2006 · SBK College, Jaisalmer, Rajasthan, INDIA

Contact Details

Phones:
Business:
(352) 273-9192
Addresses:
Business Mailing:
PO Box 100236
GAINESVILLE FL 32610
Business Street:
1149 NEWELL DR RM L3 100
GAINESVILLE FL 32610