Daniel Lee
chung-ying.lee@case.edu Research description coming soon.
Qingguang Jiang
qxj5@case.edu
My research studies focus on amyloid metabolism and inflammation of Alzheimer's Disease. Specifically, I am investigating the roles of nuclear receptors, especially PPAR and LXR, in modulating these aspects of AD.
Poster:
Q. Jiang , K. Mann, B. T. Lamb, P. Tontonoz, G. E. Landreth. LXRs suppress inflammation and ameliorate amyloid pathology in APP transgenic mice. Neurosci. Abst., 2004 (The Society for Neuroscience's 34 th Annual Meeting)
Jiang, Q. , Mandrekar, S., Zelcer, N., Reed, E., Mann, K., Lamb, B.T., Tontonoz, P., Landreth, G. E.. LXR activation enhances A b clearance through an ABCA1/apolipoprotein-dependent mechanism. Keystone symposia, Nuclear Receptors: Orphan Brothers (J7) Abstract , 2006
Shweta Mandrekar
sdm19@case.edu
Research description coming soon.
Steven Ostrowski
smo9@case.edu
Chronic use of non-steroidal anti-inflammatory drugs has been shown to reduce the incidence, age of onset, and progression of Alzheimer's Disease. However, the therapeutic doses of these effects are much higher than those needed to inhibit the classical targets of the NSAIDs, the cyclooxygenase enzymes. I have been studying the effect of NSAIDs on the Nf-kappaB pathway, which is an important pro-inflammatory transcriptional pathway. I am looking at the inhibition of Nf-kappaB nuclear translocation, which is mediated by IkappaB degredation, and at other regulated steps of Nf-kappaB dependent transcription, such as Nf-kappaB phosphorylation and acetylation, chromatin remodeling, and exchange of transcriptional repressors for transcriptional activators.
Erin Reed
egr3@case.edu
Research description coming soon.
Ivy Samuels
iss2@case.edu
Divide, Differentiate, or Die: The role of ERK2 in CNS development:
The Mitogen Activated Protein Kinases, ERK1 and ERK2 are evolutionarily conserved from yeast to human, display up to 90% homology, and are ubiquitous. The activation of these proteins stimulates transcription and translation which induce essential cellular metabolic changes required for proper CNS development, function, and survival. ERK1 and ERK2 null mouse models exhibit contrasting results however. Our lab has demonstrated that ERK1 ablation has no overt phenotype while ERK2 null animals are embryonic lethal. Therefore, we have proceeded by generating a conditional knockout of the ERK2 gene using Cre/LoxP technology. Because evidence suggests that ERK1 and ERK2 have differential and specific activities in cell cycle transition events, mitogen-activated signal transduction, and synaptic plasticity, our lab is studying how a loss of functional ERK2 in GFAP+ cells of the CNS (progenitors and astrocytes) disrupts neural development, how the loss effects the cellular metabolic activity of astrocytes, neurons and fibroblasts, and how it effects learning and memory. Both in vivo examination of transgenic brains and in vitro examination of cultured astrocytes, neurons, and fibroblasts are being utilized for determination of ERK2 specific function.
Publications:
Samuels, Ivy S., ML Seibenhener, KBW Neidigh, MW Wooten. (2001) Nerve Growth Factor Stimulates the Interaction of ZIP/p62 with Atypical PKC and Targets Endosomal Localization. J Cell Biochem 82:452-466.
Yabe, T, Samuels, I, and Schwartz JP. (2002) Bone Morphogenetic Proteins BMP-6 and BMP-7 Have Differential Effects on Survival and Neurite Outgrowth of Cerebellar Granule Cell Neurons. J Neurosci Res 68(2): 161-8.
|
