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High-probability grants
According to our matching algorithm, Leslie A.C. Blair is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1987 — 1989 |
Blair, Leslie A |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Chemospecificity in Immature Olfactory Neurons @ University of California San Diego |
0.902 |
1990 — 1992 |
Blair, Leslie A |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Function of the Mas Oncogene @ University of California San Diego
The mas oncogene has recently been shown to encode an angiotensin receptor which responds preferentially to angiotensins III and II over angiotensin I, and is found primarily in neural tissue. The aim of this proposal is to study the cellular mechanisms which mediate this response and the tumorigenic capacity of the mas gene product in normal tissue. Several approaches will be used. First, the cellular response of a sensory neuron-like cell line (NG115-401L C3) to acute and chronic application of angiotensins will be studied; this clonal cell line has been stably transfected with the mas gene. Second, the effects of point mutations in the mas gene on receptor function will be studied using the Xenopus oocyte expression system. Third, the tissue specificity and timing of expression and tumor formation will be addressed by creating transgenic mice. These studies will be done as a collaborative effort between the principal investigator, Drs. M.R. Hanley, M. Goedert and T.R. Jackson (Medical Research Council, Cambridge, England), and Drs. R. Duvoisin and S. Heinemann (Salk Institute, San Diego).
|
0.906 |
1999 — 2002 |
Blair, Leslie A |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Modulation of Neuronal Calcium Channels by Igf1
DESCRIPTION: (Applicant's Abstract) The proposed research will examine the molecular, biophysical and intracellular signaling mechanisms by which insulin-like growth factor-1 (IFG-1) rapidly regulates neuronal L-type calcium channels via activation of its receptor tyrosine kinase (RTK). RTKs are ubiquitously expressed on post-mitotic neurons, but little is known about their neuronal function(s). Our recent studies using cerebellar granule neurons demonstrate that, within seconds of activating the IGF-1/RTK, both N and L calcium channel activities alter dramatically in ways expected to increase neuroexcitability, synaptic release, and somal calcium influx, and that RTK regulation of L channels is a controlling factor in neuronal survival. Here, we will: (1) Determine the regulated sites on the channels through biochemical (mapping phosphorylation sites) and molecular biological approaches (expression of mutated channels in neuronal cell lines), using biophysical analyses to assess whether and how the IGF-1-L channel regulation is modified. (2) Identify the biophysical mechanisms of the RTK-induced modulation by single channel analysis of the cerebellar L channels. (3) Define the intracellular pathway linking the IGF-1/RTK activation to L channel modulation through transient expression of active, inactive, and constitutively active variants of signaling components in granule neurons in culture. Together, the proposed experiments will provide significant insights into the mechanisms that regulate neuroexcitability, with particular relevance to development, damage- and age-induced states of under- activity and epileptic states of over-activity.
|
0.936 |