Dr Jun Yan
Research Interests
I am a senior research officer in Professor Pam McCombe and Dr
Judith Greer's research groups. My research interest is
primarily investigating the mechanisms involved in disease
development, diagnosis and treatment ischemic stroke (IS) and
multiple sclerosis (MS).
There are two types of stroke: ischemic stroke and haemorrhagic
stroke. Our study is primarily focused on ischemic stroke, as it is
the most common type, comprising about 80% of all strokes. Ischemic
stroke is resultant either from a blood clot (thrombus) blocking
circulation or by a build-up of plaque within the arteries,
narrowing vessels and resulting in a loss of blood flow. My primary
research area is investigating the immune responses of peripheral
lymphocytes post-ischemia. We would like to know if these immune
responses contribute to either brain damage or tissue repair. We
would also like to know how these immune responses are regulated
genetically and the degree by which immune response correlates with
clinical outcome.
My research area on MS focuses on exploring the NF-B signal
transduction pathway in the development of the disease. MS is a
chronic inflammatory, demyelinating and neurodegenerative disorder
of the central nervous system (CNS). It is considered to be an
autoimmune disease mediated primarily by CD4+ T cells,
which are activated in the peripheral blood and migrate into the
CNS. The molecular basis of MS pathogenesis is not clear.
Recent studies have shown that a transcription factor, NF-B, plays
important role in autoimmune diseases progression and is involved
in the activation of lymphocytes.
NF-kB is a ubiquitous transcription factor that plays an
important role in controlling gene expression in inflammation,
immunity, cell proliferation and apoptosis, and therefore we would
like to know what role NF-B plays in MS. In mammals, NF-B
comprises a family of five protein subunits, p50, p52, RelA (p65),
c-Rel, and Rel-B. In most resting cells, hetero- or homo-
dimers of NF-B subunits are retained in an inactive form in the
cytoplasm through association with an inhibitory protein, called
IB. Exposure of cells to a variety of stimuli leads to the rapid
phosphorylation, ubiquitination, and ultimately proteolytic
degradation of IB, which frees NF-B to translocate to the nucleus
and initiate gene transcription. We wish to determine if this
pathway is dysregulated or impacted upon in MS.
Methodology in my studies:
- 1. Flow cytometry
- 2. T cell proliferation assays
- 3. Western blots
- 4. Immunocytochemistry
- 5. DNA sequencing
- 6. Tissue culture
- 7. Luciferase assays
- 8. DNA MicroArrays
Funding acknowledgement
MS Research Australia
Potential Honours Projects and Summer research
scholarships:
To investigate if NF-kB is constitutively activated in different
immune cell types from MS patients compared to healthy
controls.
To investigate if mutations in NF-kB regulatory molecules
correlate with MS.
To investigate NFKBIA promoter function in MS using in vitro
luciferase assay.
Contact details and email
Dr Jun Yan (BSc, PhD)
Senior Research Officer
University of Queensland Centre for Clinical Research
Royal Brisbane and Women's Hospital
Herston, Brisbane, QLD
Australia 4029
Tel: 061-07-3346 6019
Fax: 061-07-3346 5594
E-mail: j.yan@uq.edu.au
Key publications:
Yan, J and JM Greer. NF-κB, a Potential Therapeutic Target
for the Treatment of Multiple Sclerosis. (Review) CNS
& Neurological Disorders - Drug Targets, 2008, 7, 536-557.
Yan, J et al Immune activation in the peripheral blood of
patients with acute ischemic stroke.
J Neuroimmunol. 2009 Jan 3; 206(1-2):112-7.
Yan J et al The effect of aging on human lymphocyte subsets:
comparison of males and females
Immunity & Ageing 2010, 7:4doi:10.1186/1742-4933-7-4
Yan J et al Frequency and function of regulatory
T cells after ischaemic stroke in humans: evidence of gender
differences Increased numbers of functionally impaired
CD4+CD25+Foxp3+ T cells after ischaemic stroke. Journal of
Immunology (submitted)
Singh P., Yan J., eett al Levelevels
of phosphorylated axonal neurofilament subunit H (pNfH) are
increased acute ischemic stroke. Journal of the Neurological
Sciences 2011