tBID Homooligomerizes in the Mitochondrial Membrane to Induce Apoptosis

Grinberg, Michal; Sarig, Rachel; Zaltsman, Yehudit; Frumkin, Dan; Grammatikakis, Nicholas; Reuveny, Eitan; Gross, Atan

doi:10.1074/jbc.m104893200

Cited by 142 publications

(110 citation statements)

References 24 publications

Supporting

Mentioning

106

Contrasting

Unclassified

Order By: Relevance

“…Previously we reported that in TNFα-activated hematopoietic FL5.12 cells, p15 tBID forms a ∼45 kD cross-linkable complex at the mitochondria [74]. More recently, we demonstrated that this complex represents an interaction between tBID and mitochondrial carrier homolog 2 (Mtch2), a novel and previously uncharacterized 33 kD protein [75,76].…”

Section: Mitochondrial Carrier Homolog 2 (Mtch2)mentioning

confidence: 97%

“…It is known that tBID activates BAX via its BH3 domain, however the interaction of tBID with Mtch2 is BH3-and BAX/BAK-independent [74]. This may imply that Mtch2 serves as an anchor protein for tBID, that stably anchors and/or correctly positions tBID in the membrane, to allow the activation of BAX via its exposed BH3 domain.…”

Section: What Might Be the Function Of Mtch2?mentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

2007

Self Cite

View full text Add to dashboard Cite

Mitochondria play a pivotal role in the process of apoptosis. Alterations in mitochondrial structure and function during apoptosis are regulated by proteins of the BCL-2 family, however their exact mechanism of action is largely unknown. Mitochondrial carriers and pores play an essential role in maintaining the normal function of mitochondria, and BCL-2 family members were shown to interact with several mitochondrial carriers/pores and to affect their function. This review focuses on the involvement of several of these mitochondrial carriers/pores in the regulation of the mitochondrial death pathway.

show abstract

Section: Mitochondrial Carrier Homolog 2 (Mtch2)mentioning

confidence: 97%

Section: What Might Be the Function Of Mtch2?mentioning

confidence: 99%

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…It is possible that the localized activity of caspase-8 helps ensure that the cleavage of Bid is performed where it is functionally needed: on the surface of the mitochondria. Although Bid was first described as a cytosolic protein (Wang et al, 1996;Li et al, 1998;Luo et al, 1998), several laboratories have reported its detection at the surface of mitochondria (Esposti et al, 2001;Grinberg et al, 2002;Tafani et al, 2002). Moreover, CL promotes tBid binding to the mitochondrial outer membrane (Lutter et al, 2000;Gonzalvez et al, 2005a, b).…”

Section: Recent Advances In Understanding Apoptosis Initiationmentioning

confidence: 99%

New insights into apoptosis signaling by Apo2L/TRAIL

2010

View full text Add to dashboard Cite

“…Accordingly, Bax À/ À Bak À/À MEF are relatively resistant to t-Bid-induced cyt c release . Nevertheless, it has also been suggested that t-Bid forms membrane-inserted homotrimers that do not interact with other mitochondrial proteins (Grinberg et al, 2002). Moreover, t-Bid can form channels in planar lipid bilayers (Schendel et al, 1999) and destabilize them (Kudla et al, 2000).…”

Section: Mitochondrial Membrane Permeabilization: the Central Event Omentioning

confidence: 99%

Mitochondria as therapeutic targets for cancer chemotherapy

et al. 2006

View full text Add to dashboard Cite

Mitochondria are vital for cellular bioenergetics and play a central role in determining the point-of-no-return of the apoptotic process. As a consequence, mitochondria exert a dual function in carcinogenesis. Cancer-associated changes in cellular metabolism (the Warburg effect) influence mitochondrial function, and the invalidation of apoptosis is linked to an inhibition of mitochondrial outer membrane permeabilization (MOMP). On theoretical grounds, it is tempting to develop specific therapeutic interventions that target the mitochondrial Achilles' heel, rendering cancer cells metabolically unviable or subverting endogenous MOMP inhibitors. A variety of experimental therapeutic agents can directly target mitochondria, causing apoptosis induction. This applies to a heterogeneous collection of chemically unrelated compounds including positively charged a-helical peptides, agents designed to mimic the Bcl-2 homology domain 3 of Bcl-2-like proteins, ampholytic cations, metals and steroid-like compounds. Such MOMP inducers or facilitators can induce apoptosis by themselves (monotherapy) or facilitate apoptosis induction in combination therapies, bypassing chemoresistance against DNA-damaging agents. In addition, it is possible to design molecules that neutralize inhibitor of apoptosis proteins (IAPs) or heat shock protein 70 (HSP70). Such IAP or HSP70 inhibitors can mimic the action of mitochondrion-derived mediators (Smac/DIABLO, that is, second mitochondria-derived activator of caspases/direct inhibitor of apoptosis-binding protein with a low isoelectric point, in the case of IAPs; AIF, that is apoptosis-inducing factor, in the case of HSP70) and exert potent chemosensitizing effects.

show abstract

tBID Homooligomerizes in the Mitochondrial Membrane to Induce Apoptosis

Cited by 142 publications

References 24 publications

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

Mitochondrial carriers and pores: Key regulators of the mitochondrial apoptotic program?

New insights into apoptosis signaling by Apo2L/TRAIL

Mitochondria as therapeutic targets for cancer chemotherapy

Contact Info

Product

Resources

About