Document Type

Open Access Thesis

Embargo Period

2-1-2017

Degree Program

Molecular & Cellular Biology

Degree Type

Master of Science (M.S.)

Year Degree Awarded

2016

Month Degree Awarded

February

Advisor Name

Lisa

Advisor Middle Initial

M

Advisor Last Name

Minter

Co-advisor Name

Barbara

Co-advisor Middle Initial

A

Co-advisor Last Name

Osborne

Third Advisor Name

Wilmore

Third Advisor Middle Initial

C

Third Advisor Last Name

Webley

Abstract

The adaptive immune system is a complex network of cells that protect the body from invasion by foreign pathogens. Crucial to the function of the adaptive immune system is the activation, proliferation and differentiation of T cells in response to foreign pathogen presentation by antigen presenting cells. T cell activation is driven through different signaling pathways that are dependent on phosphorylation of substrates by kinases. In the PLC pathway that activates the il2 gene program, Protein Kinase C-q (PKCq) and Notch1 localize to the immunological synapse and help drive the signaling cascade that leads to robust T cell activation. It has been previously shown that PKCq and Notch1, both interact with the CBM complex at the immunological synapse. Additionally, PKCq and Notch1 both have specific cytoplasmic and nuclear functions that help drive the il2 gene program. Here, we demonstrate the localization of PKCq and Notch1 constructs transfected into HEK 293 cells. The use of deletion constructs of Notch1 was intended to inform us of what functional domain of Notch1 was responsible for the interaction with PKCq, however no direct interaction was demonstrated with the PKCq and Notch1 constructs used in these experiments. We hypothesize that this is likely due to the inactive form of PKCq found in our construct, or a result of the cell type used in these experiments.

Included in

Immunity Commons

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