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Full-Text Articles in Biology
Is Vdac1 A Novel Bcl2 Family Member That Binds Bax?, Claire Pearson
Is Vdac1 A Novel Bcl2 Family Member That Binds Bax?, Claire Pearson
Honors Theses
Apoptosis is a type of regulated cell death important for normal embryonic development and maintenance of adult tissues by removing excess or dysfunctional cells to ensure proper functioning of organs. The Bcl-2 family of proteins determines whether apoptosis remains suppressed or becomes activated through the balance of interactions among pro-survival and pro-death members. A defining feature of the Bcl-2 family is a BH3 domain that drives interactions between the family members. Isoform 1 of the voltage dependent anion channel (VDAC1) has an important role in metabolism, but was recently found to have high homology with known BH3 domains. This study …
Does Vdac2 Have A Bh3 Domain?, Lillian Ferkany
Does Vdac2 Have A Bh3 Domain?, Lillian Ferkany
Honors Theses
Mitochondrial outer membrane permeabilization (MOMP) by Bax oligomerization triggers apoptosis. BCl-2 family proteins, classified as BH3 only proteins, pro-survival proteins, or pro-apoptotic proteins, control apoptosis partly through their agonist or antagonistic effects on Bax, which are mediated by their conserved BH3 domains. All BH3 domains form an alpha helix containing 5-7 conserved hydrophobic residues, designated H0-H5, and one conserved aspartic acid that drive interaction with Bax and other ‘multi-domain’ BCl-2 members. BH3 agonists induce Bax oligomerization, while BH3 antagonists sequester Bax to prevent MOMP. We discovered that voltage dependent anion channels (VDACs) in the MOM contain a putative BH3-like domain …
Flow Cytometry And Biochemical Analysis Of Apoptotic Mouse Ht-2 T - Lymphocytes, Nell Pinkston
Flow Cytometry And Biochemical Analysis Of Apoptotic Mouse Ht-2 T - Lymphocytes, Nell Pinkston
Honors Theses
Apoptosis is a highly organized intracellular death program in multicellular animals. In the vertebrate immune system, apoptosis plays a central role in preventing the emergence of autoreactive lymphocytes. In this study, we used multiple stimuli (staurosporine, camptothecin, and cytokine deprivation - interleukin-2 or IL-2) to initiate apoptosis in IL-2 dependent, mouse HT-2 T-lymphocytes. All three inducers triggered DNA laddering and phosphatidylserine externalization. Propidium iodide staining and flow cytometry were also used to determine whether apoptotic cells accumulated in a specific stage of the cell cycle, and whether the mode of induction affected cell cycle distribution. Our findings indicate that IL-2 …