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Human BH3 Interacting Domain Death Agonist (BID) interaction partners

1. Differential roles for FL_BID and t-BID in Burkitt's lymphoma during apoptosis. There is a functional cooperation between BAK and BAX during VT-1-induced apoptosis and, unexpectedly, that activation of caspase-8 and production of t-BID were not mandatory for initiation of the cell death process.

2. These results identify a role for Bid in homeostatic mitochondrial cristae reorganization, that we link to human cardiac disease.

3. results suggest that histone modifications in the promoter region of miR-500a may be responsible for the increased expression of miR-500a in Hepatocellular carcinoma (HCC), which promotes cancer progression by targeting BID, indicating that miR-500a may be a potential prognostic predictor and therapeutic target for HCC patients.

4. The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production.

5. administration of SMAC or BH3 mimetics following short-term paclitaxel treatment could be an effective therapeutic strategy for TNBC, while only BH3-mimetics could effectively overcome long-term paclitaxel resistance

6. caspase-10 was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage

7. an oligomeric arrangement of Bid, Bax, and possibly other members of the Bcl-2 family of proteins that form a self-propagating network that permeabilizes the outer-mitochondrial membrane.

8. Combined therapy with Seliciclib((R)) and Belinostat((R)) results in eradication of non-small cell lung cancer via apoptosis induction and BID activation.

9. Results from genome-wide DNA methylation, functional network analysis and pyrosequencing, show selective CpG sites (NOS1AP, BID, and GABRB1) differentially methylated in smokers and chronic obstructive pulmonary disease patients compared to nonsmokers.

10. The adenovirus-mediated truncated Bid overexpression induced by the Cre/LoxP system can effectively eliminate CD133+ ovarian cancer stem cells, representing a novel therapeutic strategy for the treatment of ovarian cancer.

11. MiR-20a-directed regulation of BID in colorectal cancer.

12. the results establish that cleavage by caspase 8 and the subsequent association with the outer mitochondrial membrane are two critical events that activate Bid during death receptor-mediated apoptosis.

13. The results indicate that BID-independent pathways are responsible for FAS-dependent human islet cell death in Type 1 diabetes.

14. The BID-MTCH2 axis regulates the differentiation/apoptosis of stem cells and mitochondrial metabolism. (Review)

15. Data suggest, in models of spatial propagation of mitochondrial permeabilization during apoptosis, there appears to be requirement for cooperative signaling involving truncated-BID and ROS (reactive oxygen species) for efficient/ robust propagation.

16. this study emphasizes that the coordinated action of hGzmB-activated p53 and GzmB-cleaved Bid is important for GzmB-induced cell death and for cytotoxic lymphocyte/Natural Killer Cell-mediated killing of target cells.

17. Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.

18. Tax confers apoptosis resistance to HTLV-1-infected T cells by suppressing the expression of Bim and Bid.

19. EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid).

20. Inhibition of NANOGP8 or NANOG enhances the cytotoxicity of BH3 mimetics.

Mouse (Murine) BH3 Interacting Domain Death Agonist (BID) interaction partners

1. Bid promotes E3 ubiquitin ligase-mediated signaling downstream of TLR3 and TLR4 inducing a pro-inflammatory response.

2. These results identify a role for Bid in homeostatic mitochondrial cristae reorganization, that we link to human cardiac disease.

3. 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.

4. 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.

5. Cleaved Bid did not permeabilize the membrane, but lowered the membrane breakthrough force.

6. 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.

7. 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.

8. ATM-BID-MTCH2 pathway that we have identified plays a critical role in the DDR via regulation of mitochondrial metabolism.

9. DRP1-dependent apoptotic mitochondrial fission occurs independently of BAX, BAK and APAF1 to amplify cell death by BID and oxidative stress.

10. 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.

11. Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.

12. BID protein suppresses p38 activity and induce malignant cell transformation of hepatocytes.

13. important mediator of hepatic ischemia-reperfusion injury in both lean and steatotic livers

14. 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

15. 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.

16. 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

17. 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.

18. 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.

19. as soluble Bid progresses toward a membrane-inserted state, it undergoes an oligomerization process similar to that observed for Bax

20. 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

Zebrafish BH3 Interacting Domain Death Agonist (BID) interaction partners

1. Stage-specific expression of TNFalpha regulates bad/bid-mediated apoptosis and RIP1/ROS-mediated secondary necrosis in Birnavirus-infected fish cells.

Pig (Porcine) BH3 Interacting Domain Death Agonist (BID) interaction partners

1. Bid and Bax are signal transduction factors in granulosa cells and play proapoptotic roles.

Xenopus laevis BH3 Interacting Domain Death Agonist (BID) interaction partners

1. Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3-dependent Proteolysis of JNK1-2 and Bid.

2. tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BID and Caspases-2 and -8

3. Here, we identified and characterized the Xenopus homologs of caspase-10 (xCaspase-10beta), a novel initiator caspase, and Bid (xBid), a BH3-only molecule of the Bcl-2 family involved in both the extrinsic and intrinsic pathways.

4. In transgenic Xenopus, restricting tBID expression to the lens-forming cells enables the specific ablation of the lens without affecting the development of other eye structures.

5. diubiquitylation is a specific feature of xBid.