Area:
Neurotransmitters, Lysosomal storage disorders
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High-probability grants
According to our matching algorithm, Richard J. Reimer is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1998 — 2002 |
Reimer, Richard J |
K08Activity Code Description:
To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Vesicular Transport of Amino Acid Neurotransmitters
glutamate transporter; neurotransmitter transport; protein structure function; synaptic vesicles; membrane transport proteins; recombinant proteins; electrophysiology; biophysics; liposomes; glutamine; gene expression; neurons; protein reconstitution; Xenopus oocyte; tissue /cell culture;
|
1 |
| 2003 — 2008 |
Reimer, Richard J |
K02Activity Code Description:
Undocumented code - click on the grant title for more information. P51Activity Code Description:
To support centers which include a multidisciplinary and multi-categorical core research program using primate animals and to maintain a large and varied primate colony which is available to affiliated, collaborative, and visiting investigators for basic and applied biomedical research and training. |
Molecular Mechanisms of Vesicular Glutamate Transport @ Southwest Foundation For Biomedical Res
Address; BNPI protein; Brain; CRISP; Cell Communication; Cell Interaction; Cell-to-Cell Interaction; Cells; Chloride Channels; Computer Retrieval of Information on Scientific Projects Database; Computer information processing; Data; Encephalon; Encephalons; Funding; Glutamates; Goals; Grant; Institution; Investigators; Ion Channels, Chloride; L-Glutamate; Lead; Molecular; NIH; National Institutes of Health; National Institutes of Health (U.S.); Nature; Nerve Cells; Nerve Transmitter Substances; Nerve Unit; Nervous System, Brain; Neural Cell; Neural Transmission; Neurocyte; Neuronal Injury; Neurons; Neurotransmitters; Pb element; Phosphates; Play; Process; Processing, Information; Proteins; Regulation; Research; Research Personnel; Research Resources; Researchers; Resources; Role; Source; Structure; Synaptic Transmission; Synaptic Vesicles; United States National Institutes of Health; VESCL; VGLUT1 protein; Vesicle; brain-specific Na-dependent inorganic phosphate cotransporter; excitotoxicity; gene product; heavy metal Pb; heavy metal lead; improved; inorganic phosphate; insight; neuron injury; neuronal; protein function; social role; vesicular glutamate transporter 1
|
1 |
| 2007 — 2010 |
Reimer, Richard J |
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. |
Pathophysiology of Lysosomal Free Sialic Acid Storage Disorders
DESCRIPTION (provided by applicant): The broad, long-term goal of this proposal is to define mechanisms involved in the pathophysiology of the lysosomal storage disorders Salla disease and infantile sialic acid storage disorder (ISSD) in order to identify novel therapeutic approaches. These disorders are autosomal recessive neurodegenerative diseases associated with progressive impairment of motor function, mental retardation, and ultimately premature death. Enlarged cytoplasmic vacuoles filled with the amino sugar sialic acid define the cellular pathology and a defect in transport of sialic acid across lysosomal membranes has been described. Genetic studies have determined that several mutations in a gene encoding a single protein designated sialin are causative. However, the understanding of the function of sialin, and the physiological effect of genetic alterations is limited. Preliminary data indicate that sialin is a sialic acid transporter that resides in late- endosomal/lysosomal subcellular compartment. Data further indicate that the primary defect in these diseases is a loss of transport activity. A recently developed animal model for these disorders has been generated by the targeted disruption of the mouse sialin gene, but the characterization of these mice is limited. The three specific aims are directed at determining the specific molecular mechanisms underlying the pathology associated with mutations in sialin. The first aim is to describe the developmental and pathological features of sialin deficient mice. The second aim is to determine if loss of silain leads to a defect in the biogenesis or function of the late-endosomal/lysosomal vesicles that normally contain sialin. The third aim is to determine if loss of sialin alters the temporally regulated expression of sialylated glycoproteins or gangliosides. Progress in these aims will lead to an improved understanding of the normal function of this transport protein and insight into the pathophysiology of these diseases.
|
1 |