The long range goal of this research is to provide a better understanding
of the mechanism of movement of intracellular organelles along
microtubules. Such movement plays a special role in the process of fast
axonal transport in nerve cells. This process provides one means for the
movement of newly synthesized materials from their site of synthesis in
the body of a nerve cell to the synapse at the end of the axon. Similar
motility processes, however, also are likely to play an important roles in
all eukaryotic cells. For example, the directed movement of membranous
organelles has been implicated in the extension of the endoplasmic
reticulum and mitochondria away from the nuclear region and in the
directed movement of some classes of secretory vesicles towards the plasma
membrane.
The protein kinesin has recently been isolated and shown to be a motor for
driving movement along microtubules in the anterograde direction
(corresponding to movement in a nerve cell away from the nuclear region
and toward the periphery). The energy for this movement is derived from
hydrolysis of adenosine triphosphate (ATP), and purified kinesin has
ATPase activity which is stimulated by microtubules.
The aim of this project is to determine the detailed enzymatic mechanism
of ATP hydrolysis by the kinesin/microtubule motility system with emphasis
on how hydrolysis is coupled to movement. Recent progress indicates that
kinesin undergoes a large conformational change as a function of ionic
strength and a major component for the upcoming grant period is the
further characterization of this conformational change and its possible
significance for the regulation of kinesin. An important approach will be
the characterization of individual domains of kinesin and their
interaction. These domains will be obtained by limited proteolysis and by
expression of fragments of kinesin cDNA. Resolution of these issues will
allow a more detailed kinetic analysis to be undertaken on the forms of
kinesin which are properly activated. Extensive use will be made of steady
state and single turnover kinetics and immunological approaches. The
combined information which will be available from these studies will allow
the formulation of a detailed model for mechanism of motility induced by
kinesin and its role in cellular processes.
National Institute of Neurological Disorders and Stroke
CFDA Code
DUNS Number
052184116
UEI
U3NKNFLNQ613
G4P3TF8PFH73
KZV2XNZZN3A8
MJ5BDF8KMQ43
U9C6D6YR7P69
Project Start Date
01-April-1990
Project End Date
31-December-1997
Budget Start Date
01-January-1994
Budget End Date
31-December-1994
Project Funding Information for 1994
Total Funding
$210,261
Direct Costs
$125,346
Indirect Costs
$84,915
Year
Funding IC
FY Total Cost by IC
1994
National Institute of Neurological Disorders and Stroke
$210,261
Year
Funding IC
FY Total Cost by IC
Sub Projects
No Sub Projects information available for 2R01NS028562-04A1
Publications
Publications are associated with projects, but cannot be identified with any particular year of the project or fiscal year of funding. This is due to the continuous and cumulative nature of knowledge generation across the life of a project and the sometimes long and variable publishing timeline. Similarly, for multi-component projects, publications are associated with the parent core project and not with individual sub-projects.
No Publications available for 2R01NS028562-04A1
Patents
No Patents information available for 2R01NS028562-04A1
Outcomes
The Project Outcomes shown here are displayed verbatim as submitted by the Principal Investigator (PI) for this award. Any opinions, findings, and conclusions or recommendations expressed are those of the PI and do not necessarily reflect the views of the National Institutes of Health. NIH has not endorsed the content below.
No Outcomes available for 2R01NS028562-04A1
Clinical Studies
No Clinical Studies information available for 2R01NS028562-04A1
News and More
Related News Releases
No news release information available for 2R01NS028562-04A1
History
No Historical information available for 2R01NS028562-04A1
Similar Projects
No Similar Projects information available for 2R01NS028562-04A1