27EC Zhou, Hongxia - Thomas Jefferson University - Thomas Jefferson University
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Hongxia Zhou, PhD

Contact Dr. Zhou

1020 Locust Street
Jefferson Alumni Hall, Suite 506
Philadelphia, PA 19107

(215) 503-1037

Most Recent Peer-reviewed Publications

  1. Profiling the genes affected by pathogenic TDP-43 in astrocytes
  2. Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats
  3. Reactive astrocytes secrete lcn2 to promote neuron death
  4. Pathogenic mutation in VPS35 impairs its protection against MPP+ cytotoxicity
  5. XBP1 depletion precedes ubiquitin aggregation and Golgi fragmentation in TDP-43 transgenic rats
  6. Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats
  7. Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats
  8. Early exposure to paraquat sensitizes dopaminergic neurons to subsequent silencing of PINK1 gene expression in mice
  9. Temporal expression of mutant LRRK2 in adult rats impairs dopamine reuptake
  10. TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice
  11. FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration
  12. Sustained Expression of TDP-43 and FUS in Motor Neurons in Rodent's Lifetime
  13. Transgenic rat model of neurodegeneration caused by mutation in the TDP gene
  14. Nerve injection of viral vectors efficiently transfers transgenes into motor neurons and delivers RNAi therapy against ALS
  15. Developing tTA transgenic rats for inducible and reversible gene expression
  16. A tightly regulated Pol III promoter for synthesis of miRNA genes in tandem
  17. A construct with fluorescent indicators for conditional expression of miRNA
  18. Therapeutic gene silencing delivered by a chemically modified small interfering RNA against mutant SOD1 slows amyotrophic lateral sclerosis progression
  19. Silencing of the Pink1 gene expression by conditional RNAi does not induce dopaminergic neuron death in mice
  20. Allele-specific RNAi selectively silences mutant SOD1 and achieves significant therapeutic benefit in vivo
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