PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34263972-7 2021 Cathepsins in the cytosol cleaved Bid to generate tBid, which subsequently activated Bax to induce mitochondrial outer membrane permeabilization (MOMP). tBID 50-54 BH3 interacting domain death agonist Homo sapiens 34-37 34988150-4 2021 Methods: We incorporated the pro-apoptotic truncated BH3 interacting-domain death agonist (tBID) with the mutant ecDHFR destabilizing domain to form a novel recombinant protein as the major component of an engineered tBID-based safety switch system, which would be unstable and quickly degraded in the absence of trimethoprim (TMP) but, upon TMP treatment, should become stabilized and allow tBID to induce cell death experimentally. tBID 91-95 BH3 interacting domain death agonist Homo sapiens 53-89 34988150-4 2021 Methods: We incorporated the pro-apoptotic truncated BH3 interacting-domain death agonist (tBID) with the mutant ecDHFR destabilizing domain to form a novel recombinant protein as the major component of an engineered tBID-based safety switch system, which would be unstable and quickly degraded in the absence of trimethoprim (TMP) but, upon TMP treatment, should become stabilized and allow tBID to induce cell death experimentally. tBID 217-221 BH3 interacting domain death agonist Homo sapiens 53-89 34988150-4 2021 Methods: We incorporated the pro-apoptotic truncated BH3 interacting-domain death agonist (tBID) with the mutant ecDHFR destabilizing domain to form a novel recombinant protein as the major component of an engineered tBID-based safety switch system, which would be unstable and quickly degraded in the absence of trimethoprim (TMP) but, upon TMP treatment, should become stabilized and allow tBID to induce cell death experimentally. tBID 392-396 BH3 interacting domain death agonist Homo sapiens 53-89 29407584-6 2018 Apoptosis correlated with a decrease of phospho-ERK1/2, the accumulation of Bim and translocation of truncated Bid (tBid) and jBid. tBID 116-120 BH3 interacting domain death agonist Homo sapiens 111-114 30385739-5 2018 We therefore hypothesised that improving caspase-8 activation or sensitising mitochondria to truncated Bid (tBid) could convert non-responder GBM cell lines to responders. tBID 108-112 BH3 interacting domain death agonist Homo sapiens 103-106 29022237-8 2018 Moderate release of CTSB cleaves Bax-like BH3 protein (Bid) to become active truncated Bid (tBid). tBID 92-96 BH3 interacting domain death agonist Homo sapiens 87-90 34361006-4 2021 Here we focus on the interaction between two core Bcl-2 family members, the executor pore-forming protein Bax and the truncated form of the activator protein Bid (tBid), which we imaged at the single particle level in a mitochondria-like planar supported lipid bilayer. tBID 163-167 BH3 interacting domain death agonist Homo sapiens 158-161 30017071-2 2018 Bid and its caspase-8 cleavage product, tBid, promote the permeabilization of the mitochondrial outer membrane and sequester antiapoptotic Bcl-2 proteins to counter their cytoprotective activity. tBID 40-44 BH3 interacting domain death agonist Homo sapiens 0-3 29265109-4 2018 By using single-molecule fluorescence and Forster resonance energy transfer techniques, we showed that Bax was mainly present as monomers, dimers and tetramers in lipid bilayers, while truncated Bid (tBid) enhanced the membrane association and tetramerization of Bax. tBID 200-204 BH3 interacting domain death agonist Homo sapiens 195-198 29039326-6 2017 The two flavonoids activated caspase-8, which cleaved Bid into tBid; simultaneously, Bax transferred from cytosol into mitochondria to decrease MMP; consequentially, cytochrome c released from mitochondria activated caspase-9, and then caspase-9 activated caspase-3, which executed the apoptosis. tBID 63-67 BH3 interacting domain death agonist Homo sapiens 54-57 29167312-7 2018 Investigations into the underlying molecular mechanisms reveal that bortezomib and ketoconazole act in concert to cause the accumulation of truncated Bid (tBid). tBID 155-159 BH3 interacting domain death agonist Homo sapiens 150-153 28888620-5 2017 Moreover, Bid knockdown abrogated TNF-alpha- or TRAIL-induced ROS generation, whereas overexpression of truncated Bid (tBid) or knockdown of cytochrome c spontaneously elevated ROS production. tBID 119-123 BH3 interacting domain death agonist Homo sapiens 114-117 27509965-9 2016 There was an increased expression of truncated Bid (tBid), which indicated caspase8 proteolysis activity in Bid cleavage as its substrate in the extrinsic pathway. tBID 52-56 BH3 interacting domain death agonist Homo sapiens 47-50 27716614-2 2016 Earlier studies showed that the lysosomal aspartic protease Cathepsin D (CtsD) cleaves Bid to tBid, resulting in the amplification of the initial apoptotic cascade via mitochondrial outer membrane permeabilization (MOMP).The goal of this study was to identify further targets for CtsD that might be involved in activation upon death receptor ligation. tBID 94-98 BH3 interacting domain death agonist Homo sapiens 87-90 27053107-7 2016 By generating Bid/Bax/Bak-deficient (TKO) cells, we demonstrated that Bid is primarily cleaved by caspase 8, not by effector caspases, to give rise to truncated Bid (tBid) upon TRAIL treatment. tBID 166-170 BH3 interacting domain death agonist Homo sapiens 70-73 27053107-7 2016 By generating Bid/Bax/Bak-deficient (TKO) cells, we demonstrated that Bid is primarily cleaved by caspase 8, not by effector caspases, to give rise to truncated Bid (tBid) upon TRAIL treatment. tBID 166-170 BH3 interacting domain death agonist Homo sapiens 70-73 26699404-4 2016 Based on apparently contradictory experimental evidence, two distinct molecular mechanisms have been proposed to underlie the propagation of MOMP signals, namely a reaction-diffusion mechanism governed by anisotropies in the production of the MOMP-inducer truncated Bid (tBid), or a process that drives the spatial propagation of MOMP by sequential bursts of reactive oxygen species. tBID 271-275 BH3 interacting domain death agonist Homo sapiens 266-269 26223015-8 2015 Cathepsin B process BID to active tBID which induces the release of cytochrome C from mitochondria. tBID 34-38 BH3 interacting domain death agonist Homo sapiens 20-23 23893415-9 2013 Mutagenesis of the alpha6 helix disrupted apoptotic function because a chimera of Bak with the alpha6 derived from Bcl-2 could be activated by truncated Bid (tBid) and could form BH3:groove homodimers but could not form high molecular weight oligomers or mediate cell death. tBID 158-162 BH3 interacting domain death agonist Homo sapiens 153-156 26097873-7 2015 The sorafenib-increased cathepsin B activity induced the proteolysis of Bid into tBid that stimulates the intrinsic pathway of apoptosis characterized by mitochondrial membrane depolarization, oxygen radical generation and cytochrome c release. tBID 81-85 BH3 interacting domain death agonist Homo sapiens 72-75 24973666-6 2014 Cordycepin-induced cell death was also associated with induction of Fas and death receptor 5, activation of caspase-8, and truncation of Bid (tBid), suggesting that tBid might serve to connect activation of both the mitochondrial-mediated intrinsic and death receptor-mediated extrinsic apoptotic pathways. tBID 165-169 BH3 interacting domain death agonist Homo sapiens 137-140 24901048-3 2014 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. tBID 71-75 BH3 interacting domain death agonist Homo sapiens 49-52 24901048-3 2014 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. tBID 71-75 BH3 interacting domain death agonist Homo sapiens 66-69 26417093-4 2015 Recently, a specific V2 requirement was demonstrated for mitochondrial Bak import and truncated Bid (tBid)-induced apoptosis. tBID 101-105 BH3 interacting domain death agonist Homo sapiens 96-99 24853737-2 2014 Here, we characterized the interaction of fluorescently labeled truncated Bid (tBid) with a mitochondria-like supported lipid bilayer at the single-molecule level. tBID 79-83 BH3 interacting domain death agonist Homo sapiens 74-77 24464226-2 2014 Truncated Bid (tBid) induces Bax/Bak-dependent mitochondrial outer membrane permeability and the release of cytochrome c and Smac/Diablo. tBID 15-19 BH3 interacting domain death agonist Homo sapiens 10-13 23744079-2 2013 Full-length Bid is cleaved in response to apoptotic stimuli into two fragments, p7 and tBid (p15), that are held together by strong hydrophobic interactions until the complex binds to membranes. tBID 87-91 BH3 interacting domain death agonist Homo sapiens 12-15 23173725-6 2013 The activated forms of caspase-3 (revCasp-3) and Bid (tBid) were very effective and, therefore, analyzed after stable integration into human leukemia and murine melanoma cell lines. tBID 54-58 BH3 interacting domain death agonist Homo sapiens 49-52 23333919-7 2013 The p62/LC3b complex interacts with Fas and truncated BID (tBID) physically. tBID 59-63 BH3 interacting domain death agonist Homo sapiens 54-57 23834359-5 2013 We show that caspase-9 can cleave Bid into tBid at amino acid 59 and that this cleavage of Bid is required for ROS production following serum withdrawal. tBID 43-47 BH3 interacting domain death agonist Homo sapiens 34-37 23834359-8 2013 CONCLUSIONS: Taken together, these data suggest that caspase-9 is required for mitochondrial morphological changes and ROS production by cleaving and activating Bid into tBid. tBID 170-174 BH3 interacting domain death agonist Homo sapiens 161-164 23660334-3 2013 Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid). tBID 78-82 BH3 interacting domain death agonist Homo sapiens 73-76 23190604-3 2012 Interestingly, the concerted action of ABT-737 and TRAIL to trigger the accumulation of truncated Bid (tBid) at mitochondrial membranes is identified as a key underlying mechanism. tBID 103-107 BH3 interacting domain death agonist Homo sapiens 98-101 23190604-4 2012 ABT-737 and TRAIL cooperate to cleave BH3-interacting domain death agonist (Bid) into its active fragment tBid, leading to increased accumulation of tBid at mitochondrial membranes. tBID 106-110 BH3 interacting domain death agonist Homo sapiens 76-79 23190604-4 2012 ABT-737 and TRAIL cooperate to cleave BH3-interacting domain death agonist (Bid) into its active fragment tBid, leading to increased accumulation of tBid at mitochondrial membranes. tBID 149-153 BH3 interacting domain death agonist Homo sapiens 76-79 22761256-3 2012 We found that caspase 8-cleaved Bid (tBid) could result in LMP directly. tBID 37-41 BH3 interacting domain death agonist Homo sapiens 32-35 23019260-6 2012 Bid in the PD temporal cortex could be further cleaved into tBid in the cytosol, which is translocated into the mitochondria, where cytochrome c is then released and caspase-3 is subsequently activated. tBID 60-64 BH3 interacting domain death agonist Homo sapiens 0-3 22761256-10 2012 We further noted that chymotrypsin-cleaved Bid is more potent than tBid at binding to PA, inserting into the lipid bilayer, and promoting LMP. tBID 67-71 BH3 interacting domain death agonist Homo sapiens 43-46 22683989-2 2012 It was also shown that recruitment of mitochondria in IFN-alpha induced apoptosis involves the cleavage of BH3 interacting domain death agonist (Bid) to truncated Bid (tBid). tBID 168-172 BH3 interacting domain death agonist Homo sapiens 145-148 22683989-2 2012 It was also shown that recruitment of mitochondria in IFN-alpha induced apoptosis involves the cleavage of BH3 interacting domain death agonist (Bid) to truncated Bid (tBid). tBID 168-172 BH3 interacting domain death agonist Homo sapiens 163-166 22507272-11 2012 Apoptosis occurred with activation of caspase-8 and cleavage of Bid to tBid, increase in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and increases in the expression and activity of calpain and caspase-3. tBID 71-75 BH3 interacting domain death agonist Homo sapiens 64-67 22513214-3 2012 Combination treatment of HNSCC cells synergistically induced apoptotic cell death accompanied by caspase-8, caspase-9, and caspase-3 activation and Bid cleavage into truncated Bid (tBid). tBID 181-185 BH3 interacting domain death agonist Homo sapiens 176-179 22416135-1 2012 The molecular basis of the interaction between mitochondrial carrier homologue 2 (MTCH2) and truncated BID (tBID) was characterized. tBID 108-112 BH3 interacting domain death agonist Homo sapiens 103-106 22019693-7 2012 Moreover, the BH3-only protein Bid was cleaved into a truncated Bid (tBid) after cinobufacini treatment. tBID 69-73 BH3 interacting domain death agonist Homo sapiens 31-34 22019693-7 2012 Moreover, the BH3-only protein Bid was cleaved into a truncated Bid (tBid) after cinobufacini treatment. tBID 69-73 BH3 interacting domain death agonist Homo sapiens 64-67 22994712-8 2012 Truncated-Bid (tBid) translocated to mitochondria and activated the mitochondrial pathway in conjunction with down-regulation of Bcl-2 protein expression. tBID 15-19 BH3 interacting domain death agonist Homo sapiens 10-13 21986059-6 2012 Interestingly, Bcl-2 family member Bid was cleaved during the course of infection, and the truncated Bid (tBid) appeared to play a role in the initiation of the intrinsic apoptosis with increased release of cytochrome c in cytosol. tBID 106-110 BH3 interacting domain death agonist Homo sapiens 101-104 19777160-8 2010 Combination therapy showed activation of caspase-8, cleavage of Bid to tBid, increase in p53 and p21 expression, down regulation of anti-apoptotic Mcl-1, and increase in Bax:Bcl-2 ratio to trigger apoptosis. tBID 71-75 BH3 interacting domain death agonist Homo sapiens 64-67 21786169-6 2011 Combination therapy caused activation of caspase-8 and cleavage of Bid to tBid and increased Bax:Bcl-2 ratio and mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF). tBID 74-78 BH3 interacting domain death agonist Homo sapiens 67-70 21382479-4 2011 Truncated BID (tBID) translocates to the mitochondria, facilitates the release of cytochrome c, and activates the intrinsic pathways. tBID 15-19 BH3 interacting domain death agonist Homo sapiens 10-13 21382479-10 2011 Mutation of Cav-1 Y14 tyrosine to phenylalanine (Y14F) disrupted the hyperoxia-induced interaction between BID and Cav-1 and subsequently yielded a decreased level of tBID and resistance to hyperoxia-induced apoptosis. tBID 167-171 BH3 interacting domain death agonist Homo sapiens 107-110 21072056-4 2011 In this study, we have identified a native complex containing caspase-8 and BID on the mitochondrial membrane, and showed that death receptor activation by Fas or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced the cleavage of BID (tBID formation) within this complex. tBID 256-260 BH3 interacting domain death agonist Homo sapiens 76-79 21072056-4 2011 In this study, we have identified a native complex containing caspase-8 and BID on the mitochondrial membrane, and showed that death receptor activation by Fas or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced the cleavage of BID (tBID formation) within this complex. tBID 256-260 BH3 interacting domain death agonist Homo sapiens 251-254 21152867-2 2011 Previously, we constructed an immuno-carboxy terminal fragment of Bid (immuno-tBid) and reported its specific and effective destruction of HER2-positive tumor cells. tBID 78-82 BH3 interacting domain death agonist Homo sapiens 66-69 21223573-5 2011 We tested truncated Bid (tBid), a human pro-apoptotic protein that induces apoptosis very rapidly and efficiently, as suicide gene for gene therapy against HIV-1 infection. tBID 25-29 BH3 interacting domain death agonist Homo sapiens 20-23 20539308-5 2011 In addition, Bax and truncated-Bid (tBid) mediate a global increase in ER membrane permeability to ER luminal proteins in vitro. tBID 36-40 BH3 interacting domain death agonist Homo sapiens 31-34 21368876-2 2010 These platforms may be at the mitochondrial contact sites in which truncated Bid (tBid) has been demonstrated to be located. tBID 82-86 BH3 interacting domain death agonist Homo sapiens 77-80 21419123-7 2011 Cleavage of Bid into truncated Bid (tBid), as well as increased cytotoxic potential, were also observed. tBID 36-40 BH3 interacting domain death agonist Homo sapiens 12-15 21459798-4 2011 Mechanistic studies reveal that bortezomib profoundly enhances TRAIL-induced cleavage of Bid into tBid, accumulation of tBid in the cytosol, and its insertion into mitochondrial membranes, pointing to a concerted effect on Bid cleavage (TRAIL) and stabilization of tBid (bortezomib), which links the death receptor to the mitochondrial pathway. tBID 98-102 BH3 interacting domain death agonist Homo sapiens 89-92 20978129-7 2010 Cells lacking Apaf-1 or the pro-apoptotic BH3-only protein Bid exhibited lower levels of heat-induced Bak activation, cytochrome c release, and loss of mitochondrial membrane potential, although cleavage of Bid to truncated Bid (tBid) occurred downstream of caspase-9 activation. tBID 229-233 BH3 interacting domain death agonist Homo sapiens 59-62 20655869-1 2010 BAX cooperates with truncated BID (tBID) and Ca(2+) in permeabilizing the outer mitochondrial membrane (OMM) and releasing mitochondrial apoptogenic proteins. tBID 35-39 BH3 interacting domain death agonist Homo sapiens 30-33 19918914-2 2010 Introducing truncated Bid (tBid), a recently known member of the Bcl-2 family, eradicates cancer cells efficiently. tBID 27-31 BH3 interacting domain death agonist Homo sapiens 22-25 21666767-5 2010 ATRA plus IFN-gamma induced extrinsic pathway of apoptosis by activation of caspase-8 and cleavage of Bid to tBid and also down regulation of hTERT, c-IAP2, and survivin and upregulation of Smac/Diablo to promote apoptosis. tBID 109-113 BH3 interacting domain death agonist Homo sapiens 102-105 20371697-3 2010 EXPERIMENTAL DESIGN: Recombinant e23sFv-TD-tBID, consisting of a single-chain anti-HER2 antibody fragment linked to a human active truncated Bid by a 10-amino acid residue furin cleavage sequence, was bacterially expressed. tBID 43-47 BH3 interacting domain death agonist Homo sapiens 141-144 20404718-9 2010 Additionally, Vpr-induced cleavage of BID to tBID and suppression of BID expression prevented Vpr-induced apoptosis. tBID 45-49 BH3 interacting domain death agonist Homo sapiens 38-41 20404718-13 2010 CONCLUSIONS: These studies delineate a novel pathway of Vpr-induced apoptosis in RTEC, which is mediated by sustained ERK activation, resulting in caspase 8-mediated cleavage of BID to tBID, thereby facilitating Bax-mediated mitochondrial injury and apoptosis. tBID 185-189 BH3 interacting domain death agonist Homo sapiens 178-181 19796174-2 2009 The active C-terminal fragment of Bid (tBid) translocates to the mitochondria where it interacts with cardiolipins at contact sites and induces the release of cytochrome c by a mechanism that is not yet fully understood. tBID 39-43 BH3 interacting domain death agonist Homo sapiens 34-37 20392206-1 2010 The truncated C-terminal portion of Bid (tBid) is an important intermediate in ligand-induced apoptosis. tBID 41-45 BH3 interacting domain death agonist Homo sapiens 36-39 20392206-3 2010 Here, we provide evidence that tBid is a substrate of the ubiquitin ligase Itch, which can specifically interact with and ubiquitinate tBid, but not intact Bid. tBID 135-139 BH3 interacting domain death agonist Homo sapiens 32-35 19640637-6 2010 Bax was translocated from the cytosol to mitochondria and Bid was cleaved into its truncated form, tBid. tBID 99-103 BH3 interacting domain death agonist Homo sapiens 58-61 19758996-2 2009 Although it is well established that recruitment of mitochondria in this context involves the cleavage of Bid to truncated Bid (tBid), the precise post-mitochondrial signaling responsible for executioner caspase activation is controversial. tBID 128-132 BH3 interacting domain death agonist Homo sapiens 106-109 19758996-2 2009 Although it is well established that recruitment of mitochondria in this context involves the cleavage of Bid to truncated Bid (tBid), the precise post-mitochondrial signaling responsible for executioner caspase activation is controversial. tBID 128-132 BH3 interacting domain death agonist Homo sapiens 123-126 19381674-2 2009 The aim of this study was to investigate whether gal-1 induced activation of the death-receptor pathway in Jurkat T lymphocytes mediates apoptosis via the mitochondrial pathway linked by truncated Bid (tBid). tBID 202-206 BH3 interacting domain death agonist Homo sapiens 197-200 19820711-2 2009 We used fluorescence correlation spectroscopy to quantify the molecular interactions of BH3-interacting domain death agonist (BID) and its truncated form tBID with the B cell lymphoma extra-large protein truncated at the C terminus (BCL(XL)DeltaCt) in solution and in membranes, and we found that (i) only the active form tBID binds to BCL(XL)DeltaCt and (ii) that the membrane strongly promotes binding between them. tBID 322-326 BH3 interacting domain death agonist Homo sapiens 126-129 19820711-3 2009 Particularly, a BH3 peptide from BID disrupts the tBID-BCL(XL) complex in solution, but only partially in lipid bilayers. tBID 50-54 BH3 interacting domain death agonist Homo sapiens 33-36 19695221-8 2009 Western blotting revealed that combination therapy downregulated angiogenic factors and also induced extrinsic pathway of apoptosis with activation of caspase-8 for Bid cleavage to tBid. tBID 181-185 BH3 interacting domain death agonist Homo sapiens 165-168 19454696-6 2009 Relocalized lysosomal cathepsin B can process Bid to active tBid to cause cytochrome c and apoptosis-activating factor release from mitochondria. tBID 60-64 BH3 interacting domain death agonist Homo sapiens 46-49 19233849-5 2009 Reconstitution experiments using recombinant proteins and permeabilized Bid-deficient cells demonstrated that truncated Bid (tBid), but not full-length Bid, potently induced Bak activation and the release of cytochrome c. tBID 125-129 BH3 interacting domain death agonist Homo sapiens 72-75 19233849-5 2009 Reconstitution experiments using recombinant proteins and permeabilized Bid-deficient cells demonstrated that truncated Bid (tBid), but not full-length Bid, potently induced Bak activation and the release of cytochrome c. tBID 125-129 BH3 interacting domain death agonist Homo sapiens 120-123 19233849-5 2009 Reconstitution experiments using recombinant proteins and permeabilized Bid-deficient cells demonstrated that truncated Bid (tBid), but not full-length Bid, potently induced Bak activation and the release of cytochrome c. tBID 125-129 BH3 interacting domain death agonist Homo sapiens 120-123 19233849-9 2009 However, the fact that cleavage of Bid to tBid is mediated by executioner caspases suggests that a self-amplifying feed forward loop involving caspases, Bid, and mitochondria may help determine irreversible commitment to apoptosis. tBID 42-46 BH3 interacting domain death agonist Homo sapiens 35-38 18368485-7 2009 Also, IFN-gamma activated caspase-8 and cleaved Bid to truncated Bid (tBid) for translocation to mitochondria. tBID 70-74 BH3 interacting domain death agonist Homo sapiens 48-51 18368485-7 2009 Also, IFN-gamma activated caspase-8 and cleaved Bid to truncated Bid (tBid) for translocation to mitochondria. tBID 70-74 BH3 interacting domain death agonist Homo sapiens 65-68 18602901-6 2008 We found that 4-HPR caused apoptosis with activation of caspase-8 and cleavage of Bid to truncated Bid (tBid). tBID 104-108 BH3 interacting domain death agonist Homo sapiens 99-102 18191430-8 2008 Diclofenac also induced early Bid activation (tBid formation, 6 h), which is an upstream mechanism that initiates Bax activation and mitochondrial translocation. tBID 46-50 BH3 interacting domain death agonist Homo sapiens 30-33 18246124-4 2008 In addition, 2-ME exposure resulted in an increase in mitochondrial membrane potential, increased apoptosis, accompanied by higher activation of caspase-3, -9, cleavage of Bid to tBid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1. tBID 179-183 BH3 interacting domain death agonist Homo sapiens 172-175 18667818-8 2008 Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid). tBID 78-82 BH3 interacting domain death agonist Homo sapiens 73-76 18252800-1 2008 Truncated Bid (tBid) releases cytochrome c from mitochondria by inducing Bak (and Bax) pore formation in the outer membrane. tBID 15-19 BH3 interacting domain death agonist Homo sapiens 10-13 17765974-8 2008 Moreover, GzmH directly processes Bid to produce the active form tBid leading to cytochrome c release. tBID 65-69 BH3 interacting domain death agonist Homo sapiens 34-37 18098270-9 2008 Combination therapy activated the receptor-mediated pathway of apoptosis with induction of TNF-alpha, activation of caspase-8, and cleavage of Bid to tBid. tBID 150-154 BH3 interacting domain death agonist Homo sapiens 143-146 18173728-6 2008 The Bid cleavage coincided with a translocation of tBid from cytoplasm to mitochondria. tBID 51-55 BH3 interacting domain death agonist Homo sapiens 4-7 17440103-3 2007 Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid). tBID 223-227 BH3 interacting domain death agonist Homo sapiens 218-221 18166654-3 2007 We found that, upon Bid cleavage, the N-terminal fragment (tBid-N) is ubiquitinated and degraded, thus freeing the BH3 domain in the C-terminal fragment (tBid-C). tBID 59-63 BH3 interacting domain death agonist Homo sapiens 20-23 18166654-3 2007 We found that, upon Bid cleavage, the N-terminal fragment (tBid-N) is ubiquitinated and degraded, thus freeing the BH3 domain in the C-terminal fragment (tBid-C). tBID 154-158 BH3 interacting domain death agonist Homo sapiens 20-23 17375293-3 2007 Proteolysis of the N-terminus (encompassing H1 and H2) of Bid by caspase 8 in apoptosis yields activated "tBid" (truncated Bid), which translocates to the mitochondria and induces the efflux of cytochrome c. tBID 106-110 BH3 interacting domain death agonist Homo sapiens 58-61 17308307-6 2007 Moreover GzmK targets mitochondria by cleaving Bid to generate its active form tBid, which disrupts the outer mitochondrial membrane leading to the release of cytochrome c and endonuclease G. tBID 79-83 BH3 interacting domain death agonist Homo sapiens 47-50 17520191-1 2007 Bid, a member of the pro-apoptotic Bcl-2 protein family, is activated through caspase-8-mediated cleavage into a truncated form (p15 tBid) during TNF-alpha(tumor necrosis factor alpha)-induced apoptosis. tBID 133-137 BH3 interacting domain death agonist Homo sapiens 0-3 16888643-8 2007 Apoptosis is thought to progress via binding of truncated Bid (tBid) to mitochondrial CL, followed by CL oxidation which results in cyt. tBID 63-67 BH3 interacting domain death agonist Homo sapiens 58-61 16988947-8 2006 Activation of caspase-8 cleaved Bid to truncated Bid (tBid) in cells treated with EGC and EGCG. tBID 54-58 BH3 interacting domain death agonist Homo sapiens 32-35 17762183-8 2007 These results show that the alkaline sondition (pH=8.0) induces cell apoptosis by activating caspase-8, which cleaves Bid to tBid, tBid translocation to mitochondria, and then activating the caspase-3 in the ASTC-a-1 cells. tBID 125-129 BH3 interacting domain death agonist Homo sapiens 118-121 17154276-4 2007 In mammalian cells, cross-talk between the main apoptotic pathways (the mitochondrial and the death domain protein pathways) involve the pro-death protein BID, the active form of which, tBID, results from protease truncation and translocation to mitochondria. tBID 186-190 BH3 interacting domain death agonist Homo sapiens 155-158 16987815-2 2006 Among the "BCL-2 homology (BH) 3-only" members of pro-apoptotic proteins, truncated BID (tBID) has been implicated in direct BAX activation, although an explicit molecular mechanism remains elusive. tBID 89-93 BH3 interacting domain death agonist Homo sapiens 84-87 16987815-6 2006 Strikingly, nanomolar concentrations of a synthetic BID BH3 peptide that is chemically tethered to the liposomal membrane activated BAX almost as efficiently as tBID itself. tBID 161-165 BH3 interacting domain death agonist Homo sapiens 52-55 16987815-7 2006 These results highlight the importance of membrane targeting of the BID BH3 domain in tBID-mediated BAX activation and support a model in which tBID engages BAX to trigger its pro-apoptotic activity. tBID 86-90 BH3 interacting domain death agonist Homo sapiens 68-71 16987815-7 2006 These results highlight the importance of membrane targeting of the BID BH3 domain in tBID-mediated BAX activation and support a model in which tBID engages BAX to trigger its pro-apoptotic activity. tBID 144-148 BH3 interacting domain death agonist Homo sapiens 68-71 16988947-8 2006 Activation of caspase-8 cleaved Bid to truncated Bid (tBid) in cells treated with EGC and EGCG. tBID 54-58 BH3 interacting domain death agonist Homo sapiens 49-52 16741989-5 2006 The cleavage product of Bid, tBid, appeared in the cytosol and to a lesser extent in the mitochondria. tBID 29-33 BH3 interacting domain death agonist Homo sapiens 24-27 16708390-4 2006 The aim of our study is to evaluate the possibility of using truncated Bid (tBid) as a novel therapy for HCC treatment. tBID 76-80 BH3 interacting domain death agonist Homo sapiens 71-74 16826547-3 2006 In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c. tBID 185-189 BH3 interacting domain death agonist Homo sapiens 15-18 16826547-3 2006 In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c. tBID 231-235 BH3 interacting domain death agonist Homo sapiens 15-18 16826547-3 2006 In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c. tBID 231-235 BH3 interacting domain death agonist Homo sapiens 161-164 16826547-3 2006 In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c. tBID 185-189 BH3 interacting domain death agonist Homo sapiens 161-164 15846373-2 2005 We have evaluated changes in lipid metabolism on permeabilized hepatocytes treated with truncated Bid (tBid) in the presence of caspase inhibitors and exogenous cytochrome c. tBID 103-107 BH3 interacting domain death agonist Homo sapiens 98-101 16407197-2 2006 Caspase 8-mediated cleavage of the BH3-only protein Bid into a truncated protein (tBid) and subsequent translocation of tBid to mitochondria has been implicated in death receptor signaling. tBID 82-86 BH3 interacting domain death agonist Homo sapiens 52-55 16407197-2 2006 Caspase 8-mediated cleavage of the BH3-only protein Bid into a truncated protein (tBid) and subsequent translocation of tBid to mitochondria has been implicated in death receptor signaling. tBID 120-124 BH3 interacting domain death agonist Homo sapiens 52-55 16407197-5 2006 Cleavage of the Bid-FRET probe coincided with a translocation of tBid to the mitochondria and a collapse of the mitochondrial membrane potential (DeltaPsim). tBID 65-69 BH3 interacting domain death agonist Homo sapiens 16-19 16681997-5 2006 The continuing reduction of Bid protein and the gradual increase of tBid protein also indicated that a time-dependent increased turn-over of Bid protein into tBid. tBID 158-162 BH3 interacting domain death agonist Homo sapiens 69-72 16380381-1 2006 Engagement of death receptors such as tumor necrosis factor-R1 and Fas brings about the cleavage of cytosolic Bid to truncated Bid (tBid), which translocates to mitochondria to activate Bax/Bak, resulting in the release of cytochrome c. tBID 132-136 BH3 interacting domain death agonist Homo sapiens 110-113 16380381-1 2006 Engagement of death receptors such as tumor necrosis factor-R1 and Fas brings about the cleavage of cytosolic Bid to truncated Bid (tBid), which translocates to mitochondria to activate Bax/Bak, resulting in the release of cytochrome c. tBID 132-136 BH3 interacting domain death agonist Homo sapiens 127-130 15661737-2 2005 We show here that HN also interacts with the BH3-only Bcl-2/Bax family protein, Bid, as well as a truncated form of Bid (tBid) associated with protease-mediated activation of this proapoptotic protein. tBID 121-125 BH3 interacting domain death agonist Homo sapiens 116-119 16167168-6 2005 Recently, we have revealed that in apoptotic cells the activated/truncated form of BID, tBID, interacts with a novel, uncharacterized protein named mitochondrial carrier homolog 2 (Mtch2). tBID 88-92 BH3 interacting domain death agonist Homo sapiens 83-86 15500442-6 2005 Although the major action may reside in the C-terminus part, tBid (cleaved Bid), un-cleaved Bid also has pro-apoptotic potential when ectopically expressed in cells or in vitro. tBID 61-65 BH3 interacting domain death agonist Homo sapiens 75-78 15262979-6 2004 The expression of truncated Bid (tBid) and the reduction in mitochondrial transmembrane potential were blocked by caspase-2 or caspase-8, but not caspase-3, knockdown using an RNA interference technique. tBID 33-37 BH3 interacting domain death agonist Homo sapiens 28-31 15637055-1 2005 Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces programmed cell death through the caspase activation cascade and translocation of cleaved Bid (tBid) by the apical caspase-8 to mitochondria to induce oligomerization of multidomain Bax and Bak. tBID 167-171 BH3 interacting domain death agonist Homo sapiens 162-165 15123718-1 2004 The proapoptotic Bcl-2 family protein Bid is cleaved by caspase-8 to release the C-terminal fragment tBid, which translocates to the outer mitochondrial membrane and induces massive cytochrome c release and cell death. tBID 101-105 BH3 interacting domain death agonist Homo sapiens 38-41 15148322-4 2004 Caspase 8 cleaves full-length Bid, resulting in truncated p15 tBid. tBID 62-66 BH3 interacting domain death agonist Homo sapiens 30-33 15314281-1 2004 Bid is cleaved by caspase 8 during apoptosis and the truncated Bid (tBid) translocates to mitochondria by targeting cardiolipin. tBID 68-72 BH3 interacting domain death agonist Homo sapiens 63-66 11741882-3 2002 Using green fluorescent protein fusion proteins and immunostaining in individual permeabilized HepG2 cells, first we demonstrated that truncated Bid (15.5-kDa C-terminal fragment, tBid) evoked a rapid and essentially complete release of cytochrome c and Smac/DIABLO from every mitochondrion. tBID 180-184 BH3 interacting domain death agonist Homo sapiens 145-148 14761678-5 2004 Treatment of HepG2 cells with IH901 also induced the cleavage of cytosolic factors such as Bid and Bax and translocation of truncated Bid (tBid) to mitochondria. tBID 139-143 BH3 interacting domain death agonist Homo sapiens 134-137 12519725-1 2003 The proapoptotic activity of BID seems to solely depend upon its cleavage to truncated tBID. tBID 87-91 BH3 interacting domain death agonist Homo sapiens 29-32 12393866-5 2002 The cleavage product of Bid degradation (truncated Bid, tBid) was not detectable in the mitochondria. tBID 56-60 BH3 interacting domain death agonist Homo sapiens 24-27 14701745-4 2004 Here we show that growth factor deprivation induced proteolytic cleavage of the proapoptotic Bcl-2 family member BID to yield its active truncated form, tBID. tBID 153-157 BH3 interacting domain death agonist Homo sapiens 113-116 14701745-10 2004 These results suggest that Akt inhibits BID-mediated apoptosis downstream of BID cleavage via promotion of mitochondrial hexokinase association and antagonism of tBID-mediated BAX and BAK activation at the mitochondria. tBID 162-166 BH3 interacting domain death agonist Homo sapiens 40-43 12721291-1 2003 Caspase-8 cleaves BID to tBID, which targets mitochondria and induces oligomerization of BAX and BAK within the outer membrane, resulting in release of cytochrome c from the organelle. tBID 25-29 BH3 interacting domain death agonist Homo sapiens 18-21 12766488-3 2003 Proteolysis of the N-terminus (encompassing H1 and H2) of Bid yields activated "tBid" (truncated Bid), which translocates to the mitochondria and induces the efflux of cytochrome c. tBID 80-84 BH3 interacting domain death agonist Homo sapiens 58-61 12624108-6 2003 In these cells, Bid was processed into active forms of truncated Bid or tBid. tBID 72-76 BH3 interacting domain death agonist Homo sapiens 16-19 12624108-10 2003 Alkaline treatment stripped off tBid from the membrane-bound organellar fraction of Bid plus Bcl-2-co-transfected cells, but not from cells transfected with only Bid, suggesting inhibition of tBid insertion into mitochondrial membranes by Bcl-2. tBID 32-36 BH3 interacting domain death agonist Homo sapiens 84-87 12207176-2 2002 Bid action has been proposed to involve the mitochondrial re-location of its truncated form, tBid, to facilitate the release of apoptogenic proteins like cytochrome c. tBID 93-97 BH3 interacting domain death agonist Homo sapiens 0-3 12207176-4 2002 To advance our knowledge, this review evaluates the basic steps of Bid activation--caspase cleavage, dissociation of tBid, and lipid-mediated mitochondrial relocation--and their structure-function aspects. tBID 117-121 BH3 interacting domain death agonist Homo sapiens 67-70 12154014-3 2002 The active truncated form of BID (tBID) triggers the mitochondrial activation of caspase-9 by inducing the activation of BAK or BAX. tBID 34-38 BH3 interacting domain death agonist Homo sapiens 29-32 12154014-7 2002 We find that CK2 inhibits Apo2L/TRAIL-induced caspase-8-mediated cleavage of BID, thereby reducing the formation of tBID. tBID 116-120 BH3 interacting domain death agonist Homo sapiens 77-80 11025668-4 2000 Bid normally exists in an inactive state in the cytosol, but after cleavage by caspase 8, the carboxy-terminal portion (tBid) moves from cytosol to mitochondria, where it induces release of cytochrome c. tBID 120-124 BH3 interacting domain death agonist Homo sapiens 0-3 11752628-3 2000 The pro-apoptotic protein BID is unique in that its proteolytic cleavage product, tBID, is posttranslationally myristoylated. tBID 82-86 BH3 interacting domain death agonist Homo sapiens 26-29 11585909-2 2001 Bid action has been proposed to involve the relocation of its truncated form, tBid, to mitochondria to facilitate the release of apoptogenic cytochrome c. tBID 78-82 BH3 interacting domain death agonist Homo sapiens 0-3 11716782-2 2001 Once associated with mitochondria, truncated Bid (tBid) causes the potent release of cytochrome c, endonuclease G, and smac. tBID 50-54 BH3 interacting domain death agonist Homo sapiens 45-48 10950869-1 2000 TNFR1/Fas engagement results in the cleavage of cytosolic BID to truncated tBID, which translocates to mitochondria. tBID 75-79 BH3 interacting domain death agonist Homo sapiens 58-61 10801801-4 2000 The COOH-terminal cleavage fragment of Bid (tBid) becomes localized to mitochondrial membranes and triggers the release of cytochrome c. tBID 44-48 BH3 interacting domain death agonist Homo sapiens 39-42 9727492-2 1998 While full-length BID is localized in cytosol, truncated BID (tBID) translocates to mitochondria and thus transduces apoptotic signals from cytoplasmic membrane to mitochondria. tBID 62-66 BH3 interacting domain death agonist Homo sapiens 57-60