| The BCL-2 family member BID plays a role during embryonic development in addition to its BH3-only protein function by acting in parallel to BAX, BAK and BOK. | The BCL-2 family member BID plays a role during embryonic development in addition to its BH3-only protein function by acting in parallel to BAX, BAK and BOK.
Ke FS, Holloway S, Uren RT, Wong AW, Little MH, Kluck RM, Voss AK, Strasser A., Free PMC Article | 08/13/2022 |
| Stepwise activation of the pro-apoptotic protein Bid at mitochondrial membranes. | Stepwise activation of the pro-apoptotic protein Bid at mitochondrial membranes.
Hung CL, Chang HH, Lee SW, Chiang YW., Free PMC Article | 02/26/2022 |
| Plants expressing murine pro-apoptotic protein Bid do not have enhanced PCD. | Plants expressing murine pro-apoptotic protein Bid do not have enhanced PCD.
Manara A, Imanifard Z, Fracasso L, Bellin D, Crimi M., Free PMC Article | 06/19/2021 |
| Bid monomers lie shallowly on the lipid bilayer, where they self-assemble to form oligomers. During the initiation phase of self-assembly, the two central hydrophobic helices (alpha6 and alpha7) of Bid insert halfway into the phospholipid core, while the other helices remain on the surface. | Detection of tBid Oligomerization and Membrane Permeabilization by Graphene-Based Single-Molecule Surface-Induced Fluorescence Attenuation.
Ma L, Hu S, He X, Yang N, Chen L, Yang C, Ye F, Wei T, Li M. | 06/27/2020 |
| Bid promotes E3 ubiquitin ligase-mediated signaling downstream of TLR3 and TLR4 inducing a pro-inflammatory response. | Increased A20-E3 ubiquitin ligase interactions in bid-deficient glia attenuate TLR3- and TLR4-induced inflammation.
Kinsella S, Fichtner M, Watters O, König HG, Prehn JHM., Free PMC Article | 04/20/2019 |
| These results identify a role for Bid in homeostatic mitochondrial cristae reorganization, that we link to human cardiac disease. | Bid maintains mitochondrial cristae structure and function and protects against cardiac disease in an integrative genomics study.
Salisbury-Ruf CT, Bertram CC, Vergeade A, Lark DS, Shi Q, Heberling ML, Fortune NL, Okoye GD, Jerome WG, Wells QS, Fessel J, Moslehi J, Chen H, Roberts LJ 2nd, Boutaud O, Gamazon ER, Zinkel SS., Free PMC Article | 03/2/2019 |
| 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. | Loss of BID Delays FASL-Induced Cell Death of Mouse Neutrophils and Aggravates DSS-Induced Weight Loss.
Wicki S, Gurzeler U, Corazza N, Genitsch V, Wong WW, Kaufmann T., Free PMC Article | 09/1/2018 |
| 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. | BID links ferroptosis to mitochondrial cell death pathways.
Neitemeier S, Jelinek A, Laino V, Hoffmann L, Eisenbach I, Eying R, Ganjam GK, Dolga AM, Oppermann S, Culmsee C., Free PMC Article | 03/24/2018 |
| Cleaved Bid did not permeabilize the membrane, but lowered the membrane breakthrough force. | Pro-apoptotic cBid and Bax exhibit distinct membrane remodeling activities: An AFM study.
Unsay JD, Cosentino K, Sporbeck K, García-Sáez AJ. | 10/28/2017 |
| 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. | DNA Damage-Induced HSPC Malfunction Depends on ROS Accumulation Downstream of IFN-1 Signaling and Bid Mobilization.
Tasdogan A, Kumar S, Allies G, Bausinger J, Beckel F, Hofemeister H, Mulaw M, Madan V, Scharffetter-Kochanek K, Feuring-Buske M, Doehner K, Speit G, Stewart AF, Fehling HJ. | 07/22/2017 |
| 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. | Bid Promotes K63-Linked Polyubiquitination of Tumor Necrosis Factor Receptor Associated Factor 6 (TRAF6) and Sensitizes to Mutant SOD1-Induced Proinflammatory Signaling in Microglia.
Kinsella S, König HG, Prehn JH., Free PMC Article | 12/17/2016 |
| ATM-BID-MTCH2 pathway that we have identified plays a critical role in the DDR via regulation of mitochondrial metabolism. | The ATM-BID pathway plays a critical role in the DNA damage response by regulating mitochondria metabolism.
Gross A, Zaltsman Y, Maryanovich M., Free PMC Article | 09/10/2016 |
| DRP1-dependent apoptotic mitochondrial fission occurs independently of BAX, BAK and APAF1 to amplify cell death by BID and oxidative stress. | DRP1-dependent apoptotic mitochondrial fission occurs independently of BAX, BAK and APAF1 to amplify cell death by BID and oxidative stress.
Oettinghaus B, D'Alonzo D, Barbieri E, Restelli LM, Savoia C, Licci M, Tolnay M, Frank S, Scorrano L. | 08/20/2016 |
| 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. | An MTCH2 pathway repressing mitochondria metabolism regulates haematopoietic stem cell fate.
Maryanovich M, Zaltsman Y, Ruggiero A, Goldman A, Shachnai L, Zaidman SL, Porat Z, Golan K, Lapidot T, Gross A. | 04/16/2016 |
| Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis. | Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.
Naghdi S, Várnai P, Hajnóczky G., Free PMC Article | 01/30/2016 |
| BID protein suppresses p38 activity and induce malignant cell transformation of hepatocytes. | The BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice.
Orlik J, Schüngel S, Buitrago-Molina LE, Marhenke S, Geffers R, Endig J, Lobschat K, Rössler S, Goeppert B, Manns MP, Gross A, Vogel A. | 11/28/2015 |
| important mediator of hepatic ischemia-reperfusion injury in both lean and steatotic livers | BH3-only proteins contribute to steatotic liver ischemia-reperfusion injury.
DuBray BJ Jr, Conzen KD, Upadhya GA, Gunter KL, Jia J, Knolhoff BL, Mohanakumar T, Chapman WC, Anderson CD., Free PMC Article | 07/4/2015 |
| 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 | Distinct lipid effects on tBid and Bim activation of membrane permeabilization by pro-apoptotic Bax.
Shamas-Din A, Bindner S, Chi X, Leber B, Andrews DW, Fradin C. | 06/27/2015 |
| 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. | Differential regulation of inflammation and apoptosis in Fas-resistant hepatocyte-specific Bid-deficient mice.
Lazic M, Eguchi A, Berk MP, Povero D, Papouchado B, Mulya A, Johnson CD, Feldstein AE., Free PMC Article | 05/16/2015 |
| 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 | The BCL-2 family protein Bid is critical for pro-inflammatory signaling in astrocytes.
König HG, Coughlan KS, Kinsella S, Breen BA, Prehn JH. | 04/25/2015 |
| 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. | BID mediates selective killing of APC-deficient cells in intestinal tumor suppression by nonsteroidal antiinflammatory drugs.
Leibowitz B, Qiu W, Buchanan ME, Zou F, Vernon P, Moyer MP, Yin XM, Schoen RE, Yu J, Zhang L., Free PMC Article | 04/25/2015 |
| 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. | Multiple partners can kiss-and-run: Bax transfers between multiple membranes and permeabilizes those primed by tBid.
Shamas-Din A, Satsoura D, Khan O, Zhu W, Leber B, Fradin C, Andrews DW., Free PMC Article | 02/14/2015 |
| as soluble Bid progresses toward a membrane-inserted state, it undergoes an oligomerization process similar to that observed for Bax | The proapoptotic protein tBid forms both superficially bound and membrane-inserted oligomers.
Shivakumar S, Kurylowicz M, Hirmiz N, Manan Y, Friaa O, Shamas-Din A, Masoudian P, Leber B, Andrews DW, Fradin C., Free PMC Article | 01/3/2015 |
| 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 | Overexpression of BID in thyroids of transgenic mice increases sensitivity to iodine-induced autoimmune thyroiditis.
Wang SH, Fan Y, Baker JR Jr., Free PMC Article | 12/20/2014 |
| 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 | [Incidence of proapoptotic proteins p53 and p21 in epithelial ovarian tumors].
Gajewska M, Wielgoś M, Panek G, Marczewska J. | 05/24/2014 |