PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 cytochrome c, somatic Homo sapiens 141-153 11741882-0 2002 Rapid kinetics of tBid-induced cytochrome c and Smac/DIABLO release and mitochondrial depolarization. tBID 18-22 cytochrome c, somatic Homo sapiens 31-43 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 cytochrome c, somatic Homo sapiens 237-249 11741882-4 2002 To establish at a resolution of seconds the kinetics of tBid-induced cytochrome c and Smac/DIABLO release and depolarization, we monitored the mitochondrial membrane potential (DeltaPsi(m)) fluorimetrically in permeabilized cells and applied a rapid filtration method to obtain cytosolic fractions for Western blotting. tBID 56-60 cytochrome c, somatic Homo sapiens 69-81 11741882-5 2002 We found that subnanomolar doses of tBid were sufficient to evoke cytochrome c release and mitochondrial depolarization, whereas full-length Bid was 100-fold less effective. tBID 36-40 cytochrome c, somatic Homo sapiens 66-78 11741882-6 2002 Bcl-x(L) prevented tBid-induced cytochrome c release and depolarization. tBID 19-23 cytochrome c, somatic Homo sapiens 32-44 11741882-7 2002 In response to 2.5 nm tBid, cytochrome c release started after a 10 s delay, displayed rapid progression, and was complete at 50-70 s. Release of Smac/DIABLO was synchronized with cytochrome c release, whereas the loss of DeltaPsi(m) lagged slightly behind cytochrome c release. tBID 22-26 cytochrome c, somatic Homo sapiens 28-40 11741882-7 2002 In response to 2.5 nm tBid, cytochrome c release started after a 10 s delay, displayed rapid progression, and was complete at 50-70 s. Release of Smac/DIABLO was synchronized with cytochrome c release, whereas the loss of DeltaPsi(m) lagged slightly behind cytochrome c release. tBID 22-26 cytochrome c, somatic Homo sapiens 180-192 11741882-7 2002 In response to 2.5 nm tBid, cytochrome c release started after a 10 s delay, displayed rapid progression, and was complete at 50-70 s. Release of Smac/DIABLO was synchronized with cytochrome c release, whereas the loss of DeltaPsi(m) lagged slightly behind cytochrome c release. tBID 22-26 cytochrome c, somatic Homo sapiens 180-192 11741882-8 2002 Furthermore, tBid-induced cytochrome c release was insensitive to changes in substrate composition, but tBid-induced depolarization did not occur in the presence of extramitochondrial ATP supply. tBID 13-17 cytochrome c, somatic Homo sapiens 26-38 11741882-9 2002 Thus, tBid-induced permeabilization of the outer membrane permits rapid release of cytochrome c and Smac/DIABLO from all domains of the intermembrane space. tBID 6-10 cytochrome c, somatic Homo sapiens 83-95 11741882-10 2002 The tBid-induced loss of DeltaPsi(m) occurs after cytochrome c release and reflects impairment of oxidative metabolism. tBID 4-8 cytochrome c, somatic Homo sapiens 50-62 11782314-4 2002 We have found that the "BH3-only" molecule tBID induces a striking remodeling of mitochondrial structure with mobilization of the cytochrome c stores (approximately 85%) in cristae. tBID 43-47 cytochrome c, somatic Homo sapiens 130-142 11585909-6 2001 Secondly, native and recombinant Bid, as well as tBid, displayed lipid transfer activity under the same conditions and at the same nanomolar concentrations leading to mitochondrial relocation and release of cytochrome c. tBID 49-53 cytochrome c, somatic Homo sapiens 207-219 11716782-2 2001 Once associated with mitochondria, truncated Bid (tBid) causes the potent release of cytochrome c, endonuclease G, and smac. tBID 50-54 cytochrome c, somatic Homo sapiens 85-97 11326099-2 2001 tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. tBID 0-4 cytochrome c, somatic Homo sapiens 205-217 11326099-3 2001 We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. tBID 125-129 cytochrome c, somatic Homo sapiens 138-150 11716782-5 2001 Additionally, tBidG94E lowers the cytochrome c releasing activity of tBid without affecting its targeting to mitochondria. tBID 14-18 cytochrome c, somatic Homo sapiens 34-46 9727492-3 1998 tBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c independent of caspase activity, and then the loss of mitochondrial membrane potential, cell shrinkage, and nuclear condensation in a caspase-dependent fashion. tBID 0-4 cytochrome c, somatic Homo sapiens 83-95 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 cytochrome c, somatic Homo sapiens 190-202 10950869-0 2000 tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c. tBID 0-4 cytochrome c, somatic Homo sapiens 68-80 10950869-4 2000 Instead, we demonstrate that tBID functions as a membrane-targeted death ligand in which an intact BH3 domain is required for cytochrome c release, but not for targeting. tBID 29-33 cytochrome c, somatic Homo sapiens 126-138 10950869-5 2000 Bak-deficient mitochondria and blocking antibodies reveal tBID binds to its mitochondrial partner BAK to release cytochrome c, a process independent of permeability transition. tBID 58-62 cytochrome c, somatic Homo sapiens 113-125 10950869-6 2000 Activated tBID results in an allosteric activation of BAK, inducing its intramembranous oligomerization into a proposed pore for cytochrome c efflux, integrating the pathway from death receptors to cell demise. tBID 10-14 cytochrome c, somatic Homo sapiens 129-141 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 cytochrome c, somatic Homo sapiens 123-135 10801801-12 2000 Overexpression of stabilized tBid proteins significantly enhanced cytochrome c release and subsequent apoptosis induction approximately 2-fold compared with wild type tBid. tBID 29-33 cytochrome c, somatic Homo sapiens 66-78 10949027-3 2000 Rather, TNF-alpha induced a tBid-dependent conformational change in Bax that allowed an interaction between E1B 19K and conformationally altered Bax, which caused inhibition of cytochrome c release and caspase-9 activation. tBID 28-32 cytochrome c, somatic Homo sapiens 177-189 26223015-8 2015 Cathepsin B process BID to active tBID which induces the release of cytochrome C from mitochondria. tBID 34-38 cytochrome c, somatic Homo sapiens 68-80 28888620-7 2017 In a cell-free reconstitution system, caspase-8-mediated Bid cleavage and recombinant tBid induced mitochondrial cytochrome c release and ROS generation, which were blocked by Bcl-xL and antioxidant enzymes. tBID 86-90 cytochrome c, somatic Homo sapiens 113-125 34931711-2 2022 Here, we report that tBID can also mediate mitochondrial permeabilization by itself, resulting in release of cytochrome c and mitochondrial DNA, caspase activation and apoptosis even in absence of BAX and BAK. tBID 21-25 cytochrome c, somatic Homo sapiens 109-121 26387736-4 2015 ATR contains a BH3-like domain that allows ATR-tBid interaction at mitochondria, suppressing cytochrome c release and apoptosis. tBID 47-51 cytochrome c, somatic Homo sapiens 93-105 24292837-6 2014 Generated fragment actively participates in the core mechanism of apoptosis: it assists another product of caspase activity, tBID, in releasing cytochrome C from mitochondria. tBID 125-129 cytochrome c, somatic Homo sapiens 144-156 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 cytochrome c, somatic Homo sapiens 223-235 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 cytochrome c, somatic Homo sapiens 108-120 24141717-10 2014 Arrestin-2-(1-380) action depends on tBID: at physiological concentrations, arrestin-2-(1-380) directly binds tBID and doubles tBID-induced cytochrome C release from isolated mitochondria. tBID 37-41 cytochrome c, somatic Homo sapiens 140-152 24141717-10 2014 Arrestin-2-(1-380) action depends on tBID: at physiological concentrations, arrestin-2-(1-380) directly binds tBID and doubles tBID-induced cytochrome C release from isolated mitochondria. tBID 110-114 cytochrome c, somatic Homo sapiens 140-152 24141717-10 2014 Arrestin-2-(1-380) action depends on tBID: at physiological concentrations, arrestin-2-(1-380) directly binds tBID and doubles tBID-induced cytochrome C release from isolated mitochondria. tBID 110-114 cytochrome c, somatic Homo sapiens 140-152 23058921-6 2012 In vitro cytochrome c release experiments further confirmed that, compared with the control group, tBid treatment led to an increase in cytochrome c release from mitofilin-deficient mitochondria. tBID 99-103 cytochrome c, somatic Homo sapiens 9-21 23782464-7 2013 The Y110E mutant also showed decreased release of cytochrome c from isolated mitochondria challenged with tBid protein, resulting in a failure to activate caspase 3. tBID 106-110 cytochrome c, somatic Homo sapiens 50-62 23058921-6 2012 In vitro cytochrome c release experiments further confirmed that, compared with the control group, tBid treatment led to an increase in cytochrome c release from mitofilin-deficient mitochondria. tBID 99-103 cytochrome c, somatic Homo sapiens 136-148 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 cytochrome c, somatic Homo sapiens 207-219 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 cytochrome c, somatic Homo sapiens 132-144 21152867-7 2011 We demonstrate here that this novel immuno-tBid induces the specific destruction of HER2-overexpressing SOSP-9607-E10 cells through the release of cytochrome C. tBID 43-47 cytochrome c, somatic Homo sapiens 147-159 21382479-4 2011 Truncated BID (tBID) translocates to the mitochondria, facilitates the release of cytochrome c, and activates the intrinsic pathways. tBID 15-19 cytochrome c, somatic Homo sapiens 82-94 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 cytochrome c, somatic Homo sapiens 208-220 20978129-8 2010 Combined, the data suggest that caspase-9 is the critical initiator caspase activated during heat-induced apoptosis and that tBid may function to promote cytochrome c release during this process as part of a feed-forward amplification loop. tBID 125-129 cytochrome c, somatic Homo sapiens 154-166 20655869-4 2010 Ca(2+) in a mitochondrial permeability transition (mPT)-dependent and recombinant tBID in an mPT-independent manner promoted BAX insertion/ oligomerization in the OMM and augmented cytochrome c release. tBID 82-86 cytochrome c, somatic Homo sapiens 181-193 20850011-4 2010 Here we show that Drp1 stimulates tBid-induced Bax oligomerization and cytochrome c release by promoting tethering and hemifusion of membranes in vitro. tBID 34-38 cytochrome c, somatic Homo sapiens 71-83 19766591-5 2009 A bystander effect was also observed after exogenous expression of tBid, which facilitates MAC formation and cytochrome c release. tBID 67-71 cytochrome c, somatic Homo sapiens 109-121 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 cytochrome c, somatic Homo sapiens 159-171 19796174-3 2009 It has been shown that the alpha-helices alphaH6 and alphaH7 (which create the hairpin-forming domain of tBid) mediate the insertion of Bid into mitochondrial membranes and are essential for the cytochrome c-releasing activity. tBID 105-109 cytochrome c, somatic Homo sapiens 195-207 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 cytochrome c, somatic Homo sapiens 74-86 19228691-6 2009 CypD enhances the limiting effect of Bcl2 on the tBid-induced release of cytochrome c from mitochondria, which is not mediated via the MPT. tBID 49-53 cytochrome c, somatic Homo sapiens 73-85 19233849-8 2009 These data suggest that tBid plays an important regulatory role in the execution of DNA damage-induced cytochrome c release and apoptosis. tBID 24-28 cytochrome c, somatic Homo sapiens 103-115 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 cytochrome c, somatic Homo sapiens 30-42 18358005-1 2008 In tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, tBid is targeted to mitochondria and causes cytochrome c release. tBID 62-66 cytochrome c, somatic Homo sapiens 106-118 18358005-2 2008 We investigated the regulation of tBid-induced cytochrome c release and apoptosis by phospholipid scramblase 3 (PLS3). tBID 34-38 cytochrome c, somatic Homo sapiens 47-59 18084240-7 2008 When incubated with tBid, mitochondria isolated from U18666A-treated cells showed a delay in the release of Smac/Diablo and Cytochrome c, as well as in Bax oligomerization. tBID 20-24 cytochrome c, somatic Homo sapiens 124-136 18252800-2 2008 An important issue is whether a second tBid action, independent of Bak and Bax, is also required to enhance cytochrome c mobility in the intermembrane spaces. tBID 39-43 cytochrome c, somatic Homo sapiens 108-120 18252800-7 2008 Basal cytochrome c diffusibility in the intermembrane spaces in the absence of tBid was determined to be approximately 0.2 minute(-1), which is sufficient to support cytochrome c release with a half-time of 3.4 minutes. tBID 79-83 cytochrome c, somatic Homo sapiens 6-18 18252800-8 2008 It is concluded that tBid has a monofunctional action at low concentrations and, more generally, that the basal cytochrome c diffusibility in the intermembrane spaces is adequate for rapid and complete cytochrome c release irrespective of the mode of outer membrane permeabilisation. tBID 21-25 cytochrome c, somatic Homo sapiens 112-124 18252800-8 2008 It is concluded that tBid has a monofunctional action at low concentrations and, more generally, that the basal cytochrome c diffusibility in the intermembrane spaces is adequate for rapid and complete cytochrome c release irrespective of the mode of outer membrane permeabilisation. tBID 21-25 cytochrome c, somatic Homo sapiens 202-214 17633456-12 2007 Bax and tBid then agregate on mitochondrial membrane, which in turn causes a decrease of mitochondrial transmembrane potential and release of cytochrome C into cytoplasm. tBID 8-12 cytochrome c, somatic Homo sapiens 142-154 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 cytochrome c, somatic Homo sapiens 194-206 17375293-4 2007 The release of cytochrome c from mitochondria to the cytosol constitutes a critical control point in apoptosis that is regulated by interaction of tBid protein with mitochondrial membrane. tBID 147-151 cytochrome c, somatic Homo sapiens 15-27 17765974-8 2008 Moreover, GzmH directly processes Bid to produce the active form tBid leading to cytochrome c release. tBID 65-69 cytochrome c, somatic Homo sapiens 81-93 17520191-2 2007 Activated tBid can induce Bax oligomerization and translocation to mitochondria, triggering the release of cytochrome c, caspase-3 activation and cell apoptosis. tBID 10-14 cytochrome c, somatic Homo sapiens 107-119 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 cytochrome c, somatic Homo sapiens 159-171 17005564-2 2006 BH3-only protein, tBid, activates pro-apoptotic Bax to release cytochrome c from mitochondria. tBID 18-22 cytochrome c, somatic Homo sapiens 63-75 17440103-4 2007 Subsequently, tBid translocates to the mitochondria causing conformational changes in Bax, leading to loss of mitochondrial membrane potential and release of cytochrome c to the cytosol. tBID 14-18 cytochrome c, somatic Homo sapiens 158-170 17130128-10 2007 In isolated mitochondria, Nutlin-3 inhibited cytochrome c release induced by Ca2+, Bim peptide, and recombinant tBid. tBID 112-116 cytochrome c, somatic Homo sapiens 45-57 17005564-3 2006 tBid also activates anti-apoptotic Bcl-2 in the mitochondrial outer membrane, changing it from a single-spanning to a multispanning conformation that binds the active Bax and inhibits cytochrome c release. tBID 0-4 cytochrome c, somatic Homo sapiens 184-196 16199525-10 2005 Remarkably, recombinant Bax- or tBid-mediated release of cytochrome c from isolated mitochondria is significantly compromised in the MAP-1 knockdown cells. tBID 32-36 cytochrome c, somatic Homo sapiens 57-69 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 cytochrome c, somatic Homo sapiens 294-306 16254338-12 2005 In addition, the expression of F1L was essential to inhibit tBid-induced cytochrome c release in both wild-type murine embryonic fibroblasts (MEFs) and Bax-deficient MEFs, indicating that F1L could inhibit apoptosis in the presence and absence of Bax. tBID 60-64 cytochrome c, somatic Homo sapiens 73-85 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 cytochrome c, somatic Homo sapiens 223-235 16380381-5 2006 In vitro studies using isolated mitochondria and recombinant proteins demonstrate that Mcl-1 strongly inhibits tBid-induced cytochrome c release. tBID 111-115 cytochrome c, somatic Homo sapiens 124-136 15661737-3 2005 Synthetic HN peptide binds purified Bid and tBid in vitro and blocks tBid-induced release of cytochrome c and SMAC from isolated mitochondria, whereas mutant peptides that fail to bind Bid or tBid lack this activity. tBID 69-73 cytochrome c, somatic Homo sapiens 93-105 15661737-3 2005 Synthetic HN peptide binds purified Bid and tBid in vitro and blocks tBid-induced release of cytochrome c and SMAC from isolated mitochondria, whereas mutant peptides that fail to bind Bid or tBid lack this activity. tBID 69-73 cytochrome c, somatic Homo sapiens 93-105 15494215-9 2005 Our results suggest that the initial release of cytochrome generates tBid that is capable of translocation into the mitochondria causing further release of cytochrome c. tBID 69-73 cytochrome c, somatic Homo sapiens 156-168 15690071-5 2005 S70E expression also diminished tBid-mediated cytochrome c release and blunted chemotherapy-induced activation of caspases-9 and -3 in JM1 cells. tBID 32-36 cytochrome c, somatic Homo sapiens 46-58 15148322-5 2004 p15 tBid is potently apoptotic and activates the multidomain Bcl-2 protein, Bax, resulting in release of cytochrome c from mitochondria. tBID 4-8 cytochrome c, somatic Homo sapiens 105-117 15537572-3 2005 Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl. tBID 171-175 cytochrome c, somatic Homo sapiens 178-190 15537572-7 2005 In summary, whereas tBid permeabilizes the outer membrane to cytochrome c, Smac/DIABLO, and Omi/HtrA2, the release of cytochrome c during apoptosis will be underestimated unless sufficient ionic strength is maintained to overcome the electrostatic association of cytochrome c with membranes. tBID 20-24 cytochrome c, somatic Homo sapiens 61-73 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 cytochrome c, somatic Homo sapiens 182-194 15138279-1 2004 BCL-2 homology 3 (BH3)-only proteins of the BCL-2 family such as tBID and BIM(EL) assist BAX-type proteins to breach the permeability barrier of the outer mitochondrial membrane, thereby allowing cytoplasmic release of cytochrome c and other active inducers of cell death normally confined to the mitochondrial inter-membrane space. tBID 65-69 cytochrome c, somatic Homo sapiens 219-231 15258470-2 2004 The constitutive balanced ratio of Bax/Bcl-XL in K562 mitochondria allowed the formation of active Bax and cytochrome c release from mitochondria in the presence of a BH3-only protein, tBid, in a cell-free system. tBID 185-189 cytochrome c, somatic Homo sapiens 107-119 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 cytochrome c, somatic Homo sapiens 152-164 14500711-6 2003 Moreover, Bak-oligomerization, which is an essential event for tBid-induced cytochrome c release in the extrinsic death signaling pathway, is not associated with Noxa-induced cytochrome c release. tBID 63-67 cytochrome c, somatic Homo sapiens 76-88 14550275-4 2003 Treatment of HUVEC with angiostatin at a concentration known to inhibit cell proliferation and induce apoptosis resulted in induction of p53-, Bax-, and tBid-mediated release of cytochrome c into the cytosol. tBID 153-157 cytochrome c, somatic Homo sapiens 178-190 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 cytochrome c, somatic Homo sapiens 168-180 12846980-5 2003 Interactions between Bax and BH3 death domain proteins such as tBid result in Bax membrane integration, oligomerization, and permeabilization of the outer membrane to intermembrane proteins such as cytochrome c. tBID 63-67 cytochrome c, somatic Homo sapiens 198-210 12686415-7 2003 tBid had an opposite effect-it stimulated mitochondrial potassium uptake resulting in cytochrome c release. tBID 0-4 cytochrome c, somatic Homo sapiens 86-98 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 cytochrome c, somatic Homo sapiens 154-166 16120324-2 2003 While tBid permeabilizes the outer membrane and efficiently stimulates cytochrome c release, digitonin is unable to cause cytochrome c release in the absence of salt. tBID 6-10 cytochrome c, somatic Homo sapiens 71-83 12193163-6 2002 However, in the presence of tBid, the protein formed large complexes in mitochondrial membranes and induced the release of cytochrome c. tBID 28-32 cytochrome c, somatic Homo sapiens 123-135 12193163-8 2002 Moreover, tBid-induced Bax oligomerization was inhibited when mitochondria were pretreated with protease K. The presence of the voltage-dependent anion channel was not required either for Bax oligomerization or for Bax-induced cytochrome c release. tBID 10-14 cytochrome c, somatic Homo sapiens 227-239 12519725-5 2003 ncBID and wtBID (nc/wtBID) were much less effective than tBID in localizing to mitochondria and in inducing cytochrome c release, but only slightly less effective in inducing apoptosis. tBID 11-15 cytochrome c, somatic Homo sapiens 108-120 12082098-4 2002 The promotion of leakage by tBid is also inhibited by several substances that promote positive membrane curvature, including lysophosphatidylcholine, tritrpticin, a potent antimicrobial peptide, and cyclosporin A, a known inhibitor of cytochrome c release from mitochondria. tBID 28-32 cytochrome c, somatic Homo sapiens 235-247