VPS35 D620N Inhibits Autophagy by IGF-1R Dysregulation

Nathan Lai; Abir A. Rahman; Joshua E. Albright; Brad Morrison

VPS35 D620N Inhibits Autophagy by IGF-1R Dysregulation

Nathan Lai, Abir A. Rahman, Joshua E. Albright, Brad Morrison

Biological Sciences

Boise State University

Research output: Contribution to conference › Poster

Abstract

Parkinson’s disease (PD) is the most common motor disease in the USA and results from loss of dopaminergic (DA) neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. Recently, a PD-causing mutation in VPS35 (D620N) was reported to block autophagy. Using overexpression and shRNA-mediated gene repression, our lab has discovered evidence supporting a role for altered signlaing by the Insulin-like Growth Factor-1 Receptor (IGF-1R), a receptor known to regulate autophagy, in VPS35 D620N-expressing cells. This work may lead to the identification of new targets for PD therapy.

Original language	American English
State	Published - 1 Jul 2016
Event	Idaho Conference on Undergraduate Research 2016 - Boise State University, Boise, United States Duration: 1 Jul 2016 → …

Conference

Conference	Idaho Conference on Undergraduate Research 2016
Abbreviated title	ICUR 2016
Country/Territory	United States
City	Boise
Period	1/07/16 → …

EGS Disciplines

Molecular and Cellular Neuroscience

Cite this

@conference{471e597ab65448028ce0f2ae54b9d320,

title = "VPS35 D620N Inhibits Autophagy by IGF-1R Dysregulation",

abstract = " Parkinson{\textquoteright}s disease (PD) is the most common motor disease in the USA and results from loss of dopaminergic (DA) neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. Recently, a PD-causing mutation in VPS35 (D620N) was reported to block autophagy. Using overexpression and shRNA-mediated gene repression, our lab has discovered evidence supporting a role for altered signlaing by the Insulin-like Growth Factor-1 Receptor (IGF-1R), a receptor known to regulate autophagy, in VPS35 D620N-expressing cells. This work may lead to the identification of new targets for PD therapy.",

author = "Nathan Lai and Rahman, \{Abir A.\} and Albright, \{Joshua E.\} and Brad Morrison",

year = "2016",

month = jul,

day = "1",

language = "American English",

note = "Idaho Conference on Undergraduate Research 2016, ICUR 2016 ; Conference date: 01-07-2016",

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TY - CONF

T1 - VPS35 D620N Inhibits Autophagy by IGF-1R Dysregulation

AU - Lai, Nathan

AU - Rahman, Abir A.

AU - Albright, Joshua E.

AU - Morrison, Brad

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Parkinson’s disease (PD) is the most common motor disease in the USA and results from loss of dopaminergic (DA) neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. Recently, a PD-causing mutation in VPS35 (D620N) was reported to block autophagy. Using overexpression and shRNA-mediated gene repression, our lab has discovered evidence supporting a role for altered signlaing by the Insulin-like Growth Factor-1 Receptor (IGF-1R), a receptor known to regulate autophagy, in VPS35 D620N-expressing cells. This work may lead to the identification of new targets for PD therapy.

AB - Parkinson’s disease (PD) is the most common motor disease in the USA and results from loss of dopaminergic (DA) neurons in the substantia nigra with autophagy dysfunction being closely linked to this disease. Recently, a PD-causing mutation in VPS35 (D620N) was reported to block autophagy. Using overexpression and shRNA-mediated gene repression, our lab has discovered evidence supporting a role for altered signlaing by the Insulin-like Growth Factor-1 Receptor (IGF-1R), a receptor known to regulate autophagy, in VPS35 D620N-expressing cells. This work may lead to the identification of new targets for PD therapy.

UR - https://scholarworks.boisestate.edu/icur/2016/Poster_Session/65/

M3 - Poster

T2 - Idaho Conference on Undergraduate Research 2016

Y2 - 1 July 2016

ER -

VPS35 D620N Inhibits Autophagy by IGF-1R Dysregulation

Abstract

Conference

EGS Disciplines

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