David Huang
DavidHuangProfessorofWalterandElizaHallInstituteofMedicalResearch,Melbourne,Australia.Thelong-termgoalsofhislaboratoryaretounderstandhowcancersariseandtodevelopbetterapproachesfortheirdiagnosisandtreatment.HisfocusisontheregulationofapoptosisbytheBcl-2family.Incollaborationwithotherscientistsattheinstitute,membersofhislaboratoryareunravellingthemechanismsbywhichmembersoftheBcl-2familydeterminewhetheracelllivesordies.PreciselyhowBcl-2restrainsessentialcelldeathmediatorsBaxandBakisunclearandhowBaxandBakbecomeactivatedtodriveapoptosisisalsouncertain.Elucidatingthekeystepsincelldeathsignallingisessentialforunderstandinghowcelldeathisregulatedphysiologically.HeisactivelytranslatingtheknowledgehehsagainedsofarintoeffortstotargetBcl-2oritspro-survivalrelativesfortreatingpatientswithcancers(e.g.leukaemias,lymphomas)andidentifyingpotentialmechanismswhysuchsmallmoleculeinhibitorsmightfail.
David Huang Professor of Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.The long-term goals of his laboratory are to understand how cancers arise and to develop better approaches for their diagnosis and treatment. His focus is on the regulation of apoptosis by the Bcl-2 family.In collaboration with other scientists at the institute, members of his laboratory are unravelling the mechanisms by which members of the Bcl-2 family determine whether a cell lives or dies. Precisely how Bcl-2 restrains essential cell death mediators Bax and Bak is unclear and how Bax and Bak become activated to drive apoptosis is also uncertain. Elucidating the key steps in cell death signalling is essential for understanding how cell death is regulated physiologically.He is actively translating the knowledge he hsa gained so far into efforts to target Bcl-2 or its pro-survival relatives for treating patients with cancers (e.g. leukaemias, lymphomas) and identifying potential mechanisms why such small molecule inhibitors might fail.
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David Huang
David Huang  DavidHuangProfessorofWalterandElizaHallInstituteofMedicalResearch,Melbourne,Australia.Thelong-termgoalsofhislaboratoryaretounderstandhowcancersariseandtodevelopbetterapproachesfortheirdiagnosisandtreatment.HisfocusisontheregulationofapoptosisbytheBcl-2family.Incollaborationwithotherscientistsattheinstitute,membersofhislaboratoryareunravellingthemechanismsbywhichmembersoftheBcl-2familydeterminewhetheracelllivesordies.PreciselyhowBcl-2restrainsessentialcelldeathmediatorsBaxandBakisunclearandhowBaxandBakbecomeactivatedtodriveapoptosisisalsouncertain.Elucidatingthekeystepsincelldeathsignallingisessentialforunderstandinghowcelldeathisregulatedphysiologically.HeisactivelytranslatingtheknowledgehehsagainedsofarintoeffortstotargetBcl-2oritspro-survivalrelativesfortreatingpatientswithcancers(e.g.leukaemias,lymphomas)andidentifyingpotentialmechanismswhysuchsmallmoleculeinhibitorsmightfail.
DavidHuangProfessorofWalterandElizaHallInstituteofMedicalResearch,Melbourne,Australia.Thelong-termgoalsofhislaboratoryaretounderstandhowcancersariseandtodevelopbetterapproachesfortheirdiagnosisandtrea...
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David Huang Professor of Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.The long-term goals of his laboratory are to understand how cancers arise and to develop better approaches for their diagnosis and treatment. His focus is on the regulation of apoptosis by the Bcl-2 family.In collaboration with other scientists at the institute, members of his laboratory are unravelling the mechanisms by which members of the Bcl-2 family determine whether a cell lives or dies. Precisely how Bcl-2 restrains essential cell death mediators Bax and Bak is unclear and how Bax and Bak become activated to drive apoptosis is also uncertain. Elucidating the key steps in cell death signalling is essential for understanding how cell death is regulated physiologically.He is actively translating the knowledge he hsa gained so far into efforts to target Bcl-2 or its pro-survival relatives for treating patients with cancers (e.g. leukaemias, lymphomas) and identifying potential mechanisms why such small molecule inhibitors might fail.

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