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we show that BID is an important regulator downstream of FAS in mouse neutrophils. Loss of BID significantly delays FASL-cell death and partially counteracts the switch from apoptosis to necroptosis when caspases are blocked.
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Study exposes BID as the molecular link between the previously separated pathways of oxidative stress signaling by merging the death pathways of ferroptosis and oxytosis at the level of mitochondria, i.e. the crucial point of decision for neuronal function and survival.
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Cleaved Bid did not permeabilize the membrane, but lowered the membrane breakthrough force.
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toxic reactive oxygen species levels in Mll5(-/-) mice are critically dependent on type 1 interferon (IFN-1) signaling, which triggers mitochondrial accumulation of full-length Bid.
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In the present study, we identified the proapoptotic Bcl-2 family protein Bid as a positive regulator of mutant SOD1-induced TLR-nuclear factor-kappaB (NF-kappaB) signaling in microglia.
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ATM-BID-MTCH2 pathway that we have identified plays a critical role in the DDR via regulation of mitochondrial metabolism.
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DRP1-dependent apoptotic mitochondrial fission occurs independently of BAX, BAK and APAF1 to amplify cell death by BID and oxidative stress.
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A phosphorylation-deficient mutant of BID, MTCH2's ligand, induces an increase in OXPHOS, but with higher ROS and reduced ATP levels than Mtch2 loss, and is associated with hypersensitivity to irradiation.
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Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.
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BID protein suppresses p38 activity and induce malignant cell transformation of hepatocytes.
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important mediator of hepatic ischemia-reperfusion injury in both lean and steatotic livers
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compare membrane permeabilization by Bax activated by either cBid [cleaved Bid (p7 and p15)] or Bim and examine the role of membrane lipids in the recruitment and activation of these three Bcl-2 pro-apoptotic proteins
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Hepatocyte Bid suppression is critical for the resistance to the lethal effects of Fas activation. Fas signaling induces differential activation of non-canonical interleukin-1beta maturation, amplified in the absence of apoptotic Bid in hepatocytes.
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Data demonstrate a new role for Bid as a mediator of astrocyte activation during neuroinflammation, and suggest that Bid activation may contribute to non-cell autonomous motoneuron degeneration in amyotrophic lateral sclerosis
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BID is required for tumor suppression by NSAIDs in APCMin/+ mice. It mediates these chemopreventive effects via selective killing of APC-deficient intestinal stem cells.
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Binding to membranes is regulated by cleavage of Bid to truncated Bid (tBid), by conformation changes in tBid and Bax, and by interactions with other proteins.
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as soluble Bid progresses toward a membrane-inserted state, it undergoes an oligomerization process similar to that observed for Bax
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data demonstrate that increased thyroid expression of BID facilitates the development of autoimmune thyroiditis induced by iodine uptake. However, the overexpression of BID itself is not sufficient to initiate thyroiditis in CBA/J (H-2 k) mice
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The assessment of p53 and p21 can be expensive, but it proves to be a useful tool in difficult cases. Positive reaction to p53 can be noted in both, benign and malignant ovarian tumors
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The BH3-only proteins Bim and Bid are functionally active but are restrained by the anti-apoptotic Bcl-2 family proteins under physiological conditions.
