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S E M I N A R & V I S I T I N G S P E A K E R S E R I E S
D A T E
Wednesday, March 20th, 2019
12:00 Noon
(Followed by a trainee lunch in SR415 KIAM Bldg)
L O C A T I O N
Theatre B, Bannatyne Campus
S P E A K E R
Dr. Alyson Fournier
Professor, Faculty of Medicine
McGill University
T O P I C
Small Molecule Stabilization of protein interactions to promote axon
regeneration
Objectives:
- Define 14-3-3- adaptor proteins and small molecules targeting
these proteins
- Describe the influence of small molecules targeting 14-3-3
proteins on axon regeneration in a pre-clinical optic nerve injury model
- Discuss the mechanism used by these small molecules to promote
axon regeneration
Abstract: Damaged central nervous system (CNS) neurons have a poor ability
to spontaneously regenerate, causing persistent functional deficits after
injury. Therapies that stimulate axon growth are needed to repair CNS
damage. 14-3-3 adaptors are hub proteins that are attractive targets to
manipulate cell signaling. We have identified a positive role for 14-3-3s in
axon growth and have shown that fusicoccin-A (FC-A), a small-molecule
stabilizer of 14-3-3 protein-protein interactions, stimulates axon growth in
vitro and regeneration in vivo. Further screening of FC-A derivatives has
revealed potent axon growth-promoting compounds. Through mass
spectrometry, we find that FC-A and a potent derivative, stabilize
interactions between 14-3-3 proteins and multiple components of the Rap1
pathway to facilitate axon growth. Thus, FC-A and its derivatives exhibit
remarkable polypharmacology facilitating axon regeneration. These findings
show that 14-3-3 adaptor protein complexes are druggable targets and
identify a new class of small molecules that may be further optimized for
the repair of CNS damage
Brief Bio: Dr. Alyson Fournier (PhD) is a Professor in the Faculty of
Medicine at McGill University in Montreal, Canada. She completed her Ph.D.
in Neuroscience at McGill University (1998) and conducted her postdoctoral
training at Yale University with Dr. Strittmatter working on
neurodevelopment and regeneration. Since 2003 Dr. Fournier has led a
research lab at the Montreal Neurological Institute studying molecular
mechanisms regulating axon degeneration and regeneration. Dr. Fournier's
group studies neuronal signalling in response to acute nerve cell injury and
inflammation for the conception and validation of new therapeutic targets to
promote neuroprotection and repair.
/sent on behalf of
Tabrez Siddiqui
Chair, MNN Seminar Series
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/sent on behalf of
Ben Albensi
Hi All
Our Dementia Manitoba website is currently being updated. If you have any
new studies or reviews on Alzheimer's and/or dementia and would like to have
your lab recognized then please send me your information for posting. Or
just check out what's new and upcoming. Thanks,
http://dementiamanitoba.wixsite.com/mysite/research-blog
Dr George Perry visits the TMS and EVestG labs in Winnipeg.
Benedict C. Albensi, PhD
Dementia Research Chair
University of Manitoba & St Boniface Hospital Research
204-235-3942
Please mark your calendar
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M N N S E M I N A R & V I S I T I N G S P E A K E R S E R I E S
D A T E
Wednesday, Mar 20, 2019
12 noon
L O C A T I O N:
Theatre B
Bannatyne Campus
fourniersmall.jpgS P E A K E R
Dr. Alyson Fournier
<https://www.mcgill.ca/neuro/research/researchers/fournier>
Professor
Faculty of Medicine
McGill University
T O P I C
Small molecule stabilization of protein Interactions to promote axon
regeneration
Abstract
Damaged central nervous system (CNS) neurons have a poor ability to
spontaneously regenerate, causing persistent functional deficits after
injury. Therapies that stimulate axon growth are needed to repair CNS
damage. 14-3-3 adaptors are hub proteins that are attractive targets to
manipulate cell signaling. We have identified a positive role for 14-3-3s in
axon growth and have shown that fusicoccin-A (FC-A), a small-molecule
stabilizer of 14-3-3 protein-protein interactions, stimulates axon growth in
vitro and regeneration in vivo. Further screening of FC-A derivatives has
revealed potent axon growth-promoting compounds. Through mass
spectrometry, we find that FC-A and a potent derivative, stabilize
interactions between 14-3-3 proteins and multiple components of the Rap1
pathway to facilitate axon growth. Thus, FC-A and its derivatives exhibit
remarkable polypharmacology facilitating axon regeneration. These findings
show that 14-3-3 adaptor protein complexes are druggable targets and
identify a new class of small molecules that may be further optimized for
the repair of CNS damage
Objectives
* Define 14-3-3- adaptor proteins and small molecules targeting these
proteins
* Describe the influence of small molecules targeting 14-3-3 proteins
on axon regeneration in a pre-clinical optic nerve injury model
* Discuss the mechanism used by these small molecules to promote axon
regeneration
Short Bio
Dr. Alyson Fournier (PhD) is a Professor in the Faculty of Medicine at
McGill University in Montreal, Canada. She completed her Ph.D. in
Neuroscience at McGill University (1998) and conducted her postdoctoral
training at Yale University with Dr. Strittmatter working on
neurodevelopment and regeneration. Since 2003 Dr. Fournier has led a
research lab at the Montreal Neurological Institute studying molecular
mechanisms regulating axon degeneration and regeneration. Dr. Fourniers
group studies neuronal signalling in response to acute nerve cell injury and
inflammation for the conception and validation of new therapeutic targets to
promote neuroprotection and repair.
/sent on behalf of
Tabrez Siddiqui
Chair Seminar Series
Kelly Jorundson
Coordinator, Membership & Operations
Manitoba Neuroscience Network
Room R4046 - 351 Taché Avenue,
Winnipeg, MB R2H 2A6 CANADA
Email: kjorund(a)sbrc.ca
Tel: 204.235.3939 Fax: 204.237.4092
.
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<https://www.facebook.com/manitobaneuroscience/?fref=ts>
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<https://www.instagram.com/manitobaneuroscience/>
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/sent on behalf of
Ben Albensi
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All
We were able to record Dr. Perry's talk held on Monday Feb 4th, 2019.
Here is the link for those interested.
http://media1.cc.umanitoba.ca/legacy/bann/eos/eos_2019_02_04.mp4
Regards,
Ben
D A T E:
Monday, Feb 4, 2019
12:00 Noon
L O C A T I O N:
Theatre A Bannatyne Campus
**followed by a trainee lunch in 207 A&B Chown Bldg.
S P E A K E R:
Image result for dr george perryGeorge Perry
PhD Professor of Biology and Chemistry
Chief Scientist, Brain Health Consortium
Semmes Foundation Distinguished University Chair in Neurobiology
The University of Texas at San Antonio
T O P I C: Mitochondria At The Center Of Alzheimer's Disease
Dr. Perry's studies are focused on the mechanism of formation and
physiological consequences of the cytopathology of Alzheimer's disease. The
lab has shown that oxidative damage is the initial cytopathology in
Alzheimer's disease. They are working to determine the sequence of events
leading to neuronal oxidative damage and the source of the increased oxygen
radicals.
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/sent on behalf of
Mona Nazzal and Katinka Stecina
Subject: SCRC Journal Club Feb.8 - Nagakannan Pandian
Hello all,
For this Friday's Journal club we will have a presentation by Nagakannan
Pandian, a PhD student from the Eftekharpour lab. He will be presenting a
talk entitled "Ferroptosis in Neuronal Cell Death"
See you all on Friday! 11am to noon room 405 of Brodie Centre
-----------------------------------------------------------------------
Mona Nazzal
PhD Student
Spinal Cord Research Centre
Department of Physiology and Pathophysiology
University of Manitoba
425 BMSB-745 Bannatyne Ave
Winnipeg, MB R3E 0J9
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/sent on behalf of Dr. Ben Albensi
Everyone is invited!
D A T E:
Monday, Feb 4, 2019
12:00 Noon
L O C A T I O N:
Theatre A Bannatyne Campus
**followed by a trainee lunch in 207 A&B Chown Bldg.
S P E A K E R:
Image result for dr george perryGeorge Perry
PhD Professor of Biology and Chemistry
Chief Scientist, Brain Health Consortium
Semmes Foundation Distinguished University Chair in Neurobiology
The University of Texas at San Antonio
T O P I C: Mitochondria At The Center Of Alzheimers Disease
Dr. Perrys studies are focused on the mechanism of formation and
physiological consequences of the cytopathology of Alzheimers disease. The
lab has shown that oxidative damage is the initial cytopathology in
Alzheimers disease. They are working to determine the sequence of events
leading to neuronal oxidative damage and the source of the increased oxygen
radicals.
Kelly Jorundson
Coordinator, Membership & Operations
Manitoba Neuroscience Network
Room R4046 - 351 Taché Avenue,
Winnipeg, MB R2H 2A6 CANADA
Email: <mailto:kjorund@sbrc.ca> kjorund(a)sbrc.ca
Tel: 204.235.3939 Fax: 204.237.4092
.
******************************************
<http://www.manitobaneuroscience.ca/> cid:image003.jpg@01D159B3.9F0B9710
<https://www.facebook.com/manitobaneuroscience/?fref=ts>
cid:image007.png@01D29326.7E26D480
<https://www.instagram.com/manitobaneuroscience/>
cid:image009.jpg@01D29326.7E26D480 <https://twitter.com/manitobaneuro>
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