重组Alexa Fluor® 568荧光Anti-Bim抗体[Y36]

补充信息

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Bim also known as Bcl-2-interacting mediator of cell death is an important pro-apoptotic protein within the Bcl-2 family. It has a molecular weight of approximately 23 kDa. Bim is expressed in various tissues including the immune system nervous system and lymphoid tissues. It exists in multiple isoforms such as BimEL BimL and BimS due to alternative splicing. Bim's interaction with cellular membranes allows it to regulate apoptotic processes through mitochondrial pathways effectively.

Biological function summary

Bim regulates apoptosis by binding to pro-survival proteins like Bcl-2 and Bcl-xL releasing pro-apoptotic factors from mitochondria and activating caspases. Bim acts as part of the apoptosome complex and influences cell death regulation significantly. By promoting cytochrome c release from mitochondria Bim initiates a cascade of events leading to cell apoptosis. This regulation is vital in maintaining the balance between cell survival and death necessary for normal development and tissue homeostasis.

Pathways

Bim plays a critical role in the intrinsic apoptotic pathway. This pathway involves mitochondrial outer membrane permeabilization where Bim interacts with several Bcl-2 family proteins such as Bax and Bak to induce apoptosis. The modulation of Bim expression and activity is influenced by growth factor signaling pathways such as the PI3K-Akt pathway which affects Bim phosphorylation leading to its inactivation and subsequent degradation. Therefore Bim acts as an important node linking survival signals and apoptotic machinery.

Bim dysregulation has been implicated in conditions like cancer and autoimmune diseases. In certain cancers reduced Bim expression can result in unchecked cell proliferation and resistance to apoptosis. Conversely in autoimmune disorders overactivity of Bim may lead to excessive immune cell apoptosis contributing to disease pathogenesis. Bim's interactions with proteins like Bcl-2 and Bcl-xL are significant in cancer therapy as targeting these interactions can help overcome resistance to apoptosis in cancer cells improving treatment outcomes.