Investigating the Bax Interactome during Apoptotic Initiation (360G-Wellcome-102577_Z_13_Z)

£149,873

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