0B68 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. Heat transfer and flow characteristics during the formation of TBAB hydrate slurry
  2. Pathogenic Ubqln2 gains toxic properties to induce neuron death
  3. Profiling the genes affected by pathogenic TDP-43 in astrocytes
  4. Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats
  5. Reactive astrocytes secrete lcn2 to promote neuron death
  6. Pathogenic mutation in VPS35 impairs its protection against MPP+ cytotoxicity
  7. XBP1 depletion precedes ubiquitin aggregation and Golgi fragmentation in TDP-43 transgenic rats
  8. Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats
  9. Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats
  10. Early exposure to paraquat sensitizes dopaminergic neurons to subsequent silencing of PINK1 gene expression in mice
  11. Temporal expression of mutant LRRK2 in adult rats impairs dopamine reuptake
  12. TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice
  13. FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration
  14. Sustained Expression of TDP-43 and FUS in Motor Neurons in Rodent's Lifetime
  15. Transgenic rat model of neurodegeneration caused by mutation in the TDP gene
  16. Nerve injection of viral vectors efficiently transfers transgenes into motor neurons and delivers RNAi therapy against ALS
  17. Developing tTA transgenic rats for inducible and reversible gene expression
  18. A tightly regulated Pol III promoter for synthesis of miRNA genes in tandem
  19. A construct with fluorescent indicators for conditional expression of miRNA
  20. Therapeutic gene silencing delivered by a chemically modified small interfering RNA against mutant SOD1 slows amyotrophic lateral sclerosis progression
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