Investigating the Bax Interactome during Apoptotic Initiation (360G-Wellcome-102577_Z_13_Z)
Apoptosis is a form of programmed cell death, the avoidance of which is a hallmark of all forms of cancer. The ability to reactivate apoptosis in tumourcells therefore constitutes a rational strategy for the development of effective cancer treatments. Apoptosis is predominantly initiated in cells viathe intrinsic pathway, which is triggered by various cellular stresses and culminates in cell death following cleavage of many cellular components. This pathway is modulated by the Bcl-2 protein family, whose pro- and anti-apoptotic members react to intracellular signals and interact to determine cellular fate. If pro-apoptotic signals predominate, a Bcl-2 family member called Bax moves from the cytosol to accumulate at the mitochondria, where it causes the mitochondrial membrane to permeabilise, releasing cytotoxic molecules into the cytosol. This constitutes the point of no return for the triggering of cell death. This project will identify the various protein partners that bind to Bax during its transformative journey from quiescent cytosolic molecule to cellular executioner at the mitochondrial membrane. It will aim to characterise the binding interactions between Bax and its partners, with the goal of elucidating mechanisms of Bax activation that can be used to inform the development of novel cancer therapies.
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Grant Details
Amount Awarded | 149873 |
Applicant Surname | Rowell |
Approval Committee | PhD Studentships |
Award Date | 2013-07-15T00:00:00+00:00 |
Financial Year | 2012/13 |
Grant Programme: Title | PhD Studentship (Basic) |
Internal ID | 102577/Z/13/Z |
Lead Applicant | Mr Phil Rowell |
Partnership Value | 149873 |
Planned Dates: End Date | 2018-02-28T00:00:00+00:00 |
Planned Dates: Start Date | 2013-10-01T00:00:00+00:00 |
Recipient Org: Country | United Kingdom |
Region | Yorkshire and the Humber |
Sponsor(s) | Prof Alan Berry |