Aiqin Cao
**** ******* ** ***, ******** View, CA 94040 ( 650-***-**** (
abibns@r.postjobfree.com
Objective: Seeking for a research position in molecular biology or protein
science fields
Current position:
Work experience:
Technical proficiency:
Molecular biology
Postdoctoral Research fellow
2007-current Postdoctoral research fellow in School of medicine, Stanford
University
2002-2007 Research Assistant in Department of Horticulture and Landscape
Architecture, Purdue University
1997-2002 Research Assistant in College of Resources and Environment, South
China Agricultural University, P. R. China
DNA & RNA isolation
Electrophoresis
Site mutagenesis
SiRNA knockdown
Protein biology
Western blotting
Pull down and IP
Chip assay
Animal Techniques
Mammalians cell culture
Injection and gavage
Computer and bioinformatics
MS-Word
Sigma plot
GraphPad
Analyzing microarray data
Bacterial transformation Gene cloning
Northern&Southern blotting
Methylation
Fusion protein expression
Enzyme activity test
Elisa
Handling small animals
Excel
Photoshop
SAS
Vector construction
Real time RT-PCR
cDNA library screening
Phage Display Technology
Fusion protein purification
EMSA
Fluorescent microscopy
Handling tissue&blood samples
PowerPoint
Illustrator
Internet bioinformatics resource
Education:
. Ph.D, Department of Horticulture and Landscape Architecture,
Purdue University
. M.Sc Plant Nutritional Genetics, South China Agriculture
University, Guang Zhou, P. R. China
. B.Sc Agronomy, Hebei Agricultural University, He Bei, P. R.
China
Scholarship and honors
. 2001 "Excellent Graduate Student Award" of South China
Agriculture University
. 2000 "Excellent Master's Thesis" of South China
Agricultural University
. 1999 "Excellent Graduate Student Award" of South China
Agriculture University
. 1993-1996 First-class Scholarship and Excellent Student Award of
Hebei Agriculture
University
Publications
1. Cao A, Baldwin JC, Raghothama KG Transcriptional regulation of AtPS2, a
phosphate starvation induced putative protein phosphatase in Arabidopsis.
(Manuscript in preparation)
2. Cao A, Liu J Cytokine oncostatin M affect lipid metabolism through
multiple pathways. (manuscript in preparation)
3. Wu M, Cao A, Dong B, Liu J Reduction of serum triglycerides and free
fatty acids by liver-targeted expression of long chain Acyl-CoA synthetase
3. (Manuscript in preparation)
4. Cao A, Wu m, Li H, Liu J (2010) Janus kinase activation by cytokine
oncostatin M decreases
PCSK9 expression in liver cells. Journal of Lipid Research (accepted)
5. Dong B, Wu M, Cao A, Li H and Liu J, Suppression of Idol expression is
one additional mechanism underlying statin-induced upregulation of hepatic
LDL receptor expression. Int J Mol Med. (accepted)
6. Cao A, Li H, Zhou Y, Wu M, Liu J (2010) Long chain acyl-CoA synthetase-3
is a molecular target for peroxisome proliferator-activated receptor delta
in HepG2 hepatoma cells. J Biol Chem. 28;285(22):16664-74. Epub 2010 Mar 22
7. Liu H, Fenollar-Ferrer C, Cao A, Anselmi C, Carloni P, Liu J (2009)
Molecular dissection of human oncostatin M-mediated signal transductions
through site-directed mutagenesis. Int J Mol Med. 23(2):161-72
8. Liu J, Liu H, Fenollar-Ferrer, Cao A, Anselmi C, Carloni P (2008)
Molecular Dissection of Human Oncostatin M-Mediated Signal Transductions
Through Site-Directed Mutagenesis. Circulation: 118:S_571-S_572
9. Baldwin JC, Karthikeyan AS, Cao A, Raghothama KG (2008) Biochemical
and Molecular Analysis of LePS2;1: a Phosphate Starvation Induced Protein
Phosphatase Gene from Tomato. Planta 228 (2): 273-280
10. Cao A, Jain A, Baldwin JC, Raghothama KG (2007) Phosphate
differentially regulates 14-3-3 family members and GRF9 plays a role in Pi-
starvation induced modulation of metabolic pathways in Arabidopsis. Planta
226(5): 1219-1230
11. Jain A, Cao A, Karthikeyan AS, Baldwin JC, Raghothama KG (2005)
Phosphate deficiency suppresses expression of light-regulated psbO and psbP
genes encoding extrinsic proteins of oxygen-evolving complex of PSII.
Current Science 89(9): 1592-1596
Cao A, Liao H, and Yan X (2002) Root architectural responses to low P
availability in the soil in relation to P efficiency in common bean, Acta
Pedologica Sinica, 38(2):276-281 (in Chinese)
12. Liao H, Gerardo R, Yan X, Cao A, Brown KM, Lynch JP (2001) Effect of
phosphorus availability on basal root shallowness in common bean, Plant and
Soil 232:69-79
13. Cao A, Yan X (2001) Adaptation of soybean root architecture under
different P conditions, Journal of South China Agriculture University,
22(1): 92 (in Chinese)
14. Cao A, Liao H Yan X (2001) A simple method to quantify root
architectural changes induced by P deficiency in common bean, Plant
Nutrition and Fertilizer Sciences, 17(1): 113-116(in Chinese)
Meeting abstracts and posters
1. Cao A, Jain A, Baldwin JC, Raghothama KG (2007) Phosphate starvation
induced differential regulation of phylogenetically distinct members of
Arabidopsis 14-3-3 family indicates functional specificity, ASPB meeting
abstract
2. Baldwin JC, Karthikeyan AS, Cao A, Raghothama KG (2005) Functional
characterization and genomic analysis of a phosphate starvation induced
phosphatase gene family in Arabidopsis (AtPS2) and tomato (LePS2). ASPB
meeting abstract
3. Cao A, Baldwin JC, Jain A, Raghothama KG (2004) Are 14-3-3 genes
involved in phosphate starvation response of plants? 2004 GRC on Biology
of 14-3-3 Proteins
4. Yan X, Liao H, Cao A, He Y (2001) The role of root architecture in P
acquisition efficiency of different root systems: a case study with common
bean and rice. In: W.J. Horst et al., eds., Plant Nutrition-Food Security
and Sustainability of Agro-Ecosystems, Kluwer Academic Publishers, pp590-
591
5. Yan X, Liao H, Cao A et al. (2000) Adaptive changes in root architecture
of common bean in response to phosphorus deficiency: from computer
modeling to field observation, Proceedings of International Symposium on P
in the Soil-Plant Continumn, Beijing, 2000
Academic research experience
. Postdoctoral research
As a postdoctoral fellow, I am capable of performing experimental design,
data analysis and scientific presentation. I design and perform the
experiment independently as well as under my supervisor's guiding. I have
the strength and the ability to work independently and also comfortable
with working in team. Besides the research, I am also the safety manager of
the lab and do the ordering for the lab. The following are the main
outcomes of my research during this period of time.
1. Molecular Dissection of Human Oncostatin M-Mediated Signal Transductions
Through Site-Directed Mutagenesis: The binding of oncostatin M (OM) to type
I and type II receptor complexes elicits various biological responses by
activating MEK/ERK and JAK/STAT signaling pathways. Some OM effects are
clinically desirable such as reducing hyperlipidemia through the activation
of hepatic LDL receptor transcription, a downstream event of ERK
activation. By conducting site-directed mutagenesis, bioassays and
molecular modeling we have defined 4 OM residues that are differently
involved in the activation of ERK or STAT signaling pathway in HepG2 cells.
The results provide a structural basis of OM-mediated signaling and suggest
a potential to improve OM therapeutic properties via structural
modification.
2. Long chain acyl-CoA synthetase-3 is a molecular target for peroxisome
proliferator-activated receptor delta: ACSL3 was transcriptionally
upregulated by the cytokine oncostatin M (OSM) in HepG2 cells, accompanied
by reduced cellular triglyceride content and enhanced ?-oxidation. The
molecular mechanism underlying the OSM-induced activation of ACSL3 gene
transcription in HepG2 cells was investigated. OSM treatment resulted in a
coordinated elevation of mRNA levels of ACSL3 and peroxisome proliferator-
activated receptor ? (PPAR?). The effect of OSM on ACSL3 mRNA expression
was inhibited by cellular depletion of PPAR?. Analysis of the ACSL3
promoter sequence identified two imperfect PPAR-responsive elements (PPRE)
located in the ACSL3 promoter region -944 to -915, relative to the
transcription start site. The upregulation of ACSL3 promoter activity by
PPAR? was abolished by deletion of this PPRE-containing region or mutation
to disrupt the binding sites. Direct interactions of PPAR? with ACSL3-PPRE
sequences were demonstrated by gel mobility shift and chromatin
immunoprecipitation assays. Activation of PPAR? by L165041 in hamsters
increased ACSL3 mRNA and protein levels in the liver
3. OM regulate Proprotein convertase subtilisin/kexin type 9 (PCSK9)
through multiple pathways: PCSK9is a secreted protein that regulates
hepatic low density lipoprotein receptor (LDLR) levels. In human, PCSK9
accelerates the degradation of hepatic LDLR thus increases the levels of
circulating LDL-cholesterol. We explored that PCSK9 is regulated by
cytokine Oncostatin M (OM). In HepG2 cells, OM suppress PCSK9 expression
time and dose dependent at both mRNA and protein level. SiRNA knockdown of
PCSK9 increased the basal level of LDLR mRNA and protein and the OM
induction effect on LDLR is reduced. The binding of human OM to type I and
type II receptor complex elicits various biological responses by activating
ERK and STAT signaling pathways. Inhibitors (inhibit JAK or ERK) and SiRNA
knockdown of JAK, MEK or STAT indicate that OM regulate PCSK9 expression
may through both JAK-STAT and ERK pathway.
4. Microarray: Compare the gene expression pattern in HepG2 cells treated
with OM and U compounds, which is an ERK inhibitor. Understand the global
change of gene expression regulated by OM. Results indicated that OM
changes the main genes for lipid metabolism such as fatty acid synthesis, ?
oxidation. These genes are regulated both ERK dependent and independent
way.
. Research during Ph.D Functional analysis of phosphate starvation-
induced protein phosphatase and a general regulation factor (14-3-3)
in plants
Main outcomes: Plants develop a host of morphological, physiological and
biochemical adaptations to overcome persistent deficiency of phosphate
(Pi). The molecular basis for these adaptations is the coordinated
modulation of genes that may involve protein phosphorylation and
dephosphorylation. In my PhD study, two gene families involved in protein
phosphorylation and dephosphorylation; a putative protein phosphatase (PS2)
and a plant general regulatory factor (14-3-3), were characterized by using
reporter genes (?-glucuronidase and green fluorescent protein) and gene
knockout and over-expression Arabidopsis or tomato lines. The outcome of
this research shows that two key molecular determinants, whose expressions
are altered could play a significant role in plant adaptation to Pi
deficiency.
. Research during M.Sc Adaptive changes of some root architectural
indices in common bean in relation to phosphate efficiency
Main outcomes: Low phosphorus (P) availability is a primary abiotic stress
for common bean (Phaseolus vulgaris L.) production. Genetic improvement of
P efficiency by introducing and breeding genotypes that can grow and yield
at low P availability would be an economical and practical solution to P
deficiency. For my MS study, bean genotypes representing different origins
and ecotypic races were compared in paper pouch, stratified mesh soil pot
culture and the field. Some root architectural parameters including average
basal root growth angle, distribution and relative distribution of basal
root in top layers of the growth medium were quantified with computer image
analysis.(The results indicated a significant genotypic variation for low P
tolerance in the tested germplasm. The genetic potential of root
architecture provides the possibility of selecting this trait for improving
P acquisition efficiency in common bean. The results also demonstrate the
successful employment of the stratified mesh soil pot culture system to
study root architecture. The stratified P paper pouch system had proven its
simplicity and good correlation with the field experiment, hence is
recommended as a simple and rapid method to quantify root architectural
changes induced by P deficiency in common bean and other species.