BID

Last update 08 May 2025

Basic Info

Synonyms

BH3 interacting domain death agonist, BH3-interacting domain death agonist, BH3-interacting domain death agonist p11

+ [7]

Introduction

Induces caspases and apoptosis (PubMed:14583606). Counters the protective effect of BCL2 (By similarity). Induces ICE-like proteases and apoptosis. Induces ICE-like proteases and apoptosis. Does not induce apoptosis. Induces ICE-like proteases and apoptosis. Induces caspase activation and apoptosis (PubMed:15661737, PubMed:32029622). Allows the release of cytochrome c (PubMed:32029622).

100 Clinical Results associated with BID

100 Translational Medicine associated with BID

0 Patents (Medical) associated with BID

3,582

Literatures (Medical) associated with BID

31 Dec 2025·Pharmaceutical Biology

Apium graveolens L. alleviates acute lung injury in human A-549 cells by reducing NF-κB and NLRP3 inflammasome signaling

Article

Author: Hsieh, Shu-Ling ; Lin, Ssu-Jung ; Hsieh, Lan-Chi ; Huang, Yi-Chun ; Chi, Hsing-Yu ; Ping, Tsu-Ni ; Wu, Chih-Chung

BACKGROUNDApium graveolens L. (celery) is a dietary vegetable with anti-inflammatory properties. It has the potential to treat acute lung injury (ALI) caused by COVID-19 or other diseases.OBJECTIVETo investigate the effects of Apium graveolens water extract (AGWE) on ALI in human lung A-549 cells induced by lipopolysaccharide (LPS).MATERIALS AND METHODSA-549 cells were treated with AGWE for 24 h and then stimulated with 10 μg/mL LPS for another 24 h. The effects of AGWE on cell viability, the inflammatory response, oxidative stress, and apoptosis and their regulatory factors, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and NLR family pyrin domain containing 3 (NLRP3) inflammasome signaling activation were analyzed.RESULTSTreatment with 5-50 μg/mL AGWE reversed the decrease in cell viability caused by LPS (p < 0.05). AGWE can reduce interleukin (IL)-1β, IL-6, IL-18, and TNF-α levels; their EC₅₀ values are 61.4, 65.7, 37.8, and 79.7 μg/mL, respectively. AGWE can reduce reactive oxygen species and thiobarbituric acid reactive substances in A-549 cells induced by LPS. AGWE also reduced the levels of apoptosis (EC50 of 74.8 μg/mL) and its regulators (Bid; Caspase-9, -8, and -3; Bax) and increased the levels of the mitochondrial membrane potential in A-549 cells induced by LPS. AGWE can also decrease the protein levels of NLRP3 and Caspase-1 and the activation of NF-κB signaling in A-549 cells induced by LPS.CONCLUSIONSThese results show that 10 and 50 μg/mL AGWE can reduce the acute inflammation induced by LPS by reducing NF-κB and NLRP3 inflammasome signaling and mitochondria-dependent apoptosis pathways.

01 May 2025·Pigment Cell & Melanoma Research

PURPL Represses Radiation‐Induced Apoptosis to Promote Radioresistance in Cutaneous Melanoma by Direct Interfering With BID Cleavage

Article

Author: Wang, Ke ; Zhang, Chunting ; Li, Xue ; Han, Shuo ; Ma, Li ; Liang, Xiaoting ; Xu, Minna ; Jin, Yi ; Zhou, Liang ; Liu, Jiabin ; Liu, Jieyu

ABSTRACTThe rise of radioresistance in treating cutaneous melanoma challenges the efficacy of radiotherapy. Transcriptomic sequencing highlights PURPL as one of the top upregulated long noncoding RNAs in response to ionizing radiation (IR) treatment in melanoma cells, suggesting its role in radioresistance. To explore such hypothesis, loss‐of‐function experiments were conducted to assess the impact of PURPL on melanoma cell viability, colony formation, and migration. Mechanistic studies using RNA pulldown identified BID as the interacting protein partner of PURPL. Further analysis explored the relationship among PURPL, BID, and Caspase‐8 in the context of IR‐induced DNA damage and apoptosis through loss‐of‐ and gain‐of‐function experiments. The findings demonstrated that silencing PURPL significantly repressed melanoma cell viability, colony formation, migration, and invasiveness, indicating its potential role in promoting radioresistance. Moreover, PURPL was shown to repress IR‐induced DNA damage and apoptosis, supporting its involvement in melanoma radioresistance. Mechanistically, PURPL inhibited the interaction between BID and Caspase‐8, thereby modulating the mitochondrial apoptosis pathway and promoting radioresistance. In conclusion, this study provides evidence supporting the pro‐radioresistance role of PURPL in melanoma. In vivo assays further corroborated the in vitro findings, highlighting the potential clinical relevance of targeting PURPL in radioresistant melanoma. By interfering with the association between BID and Caspase‐8, PURPL may serve as a novel therapeutic target for clinical radiotherapy during the treatment of melanoma.

24 Apr 2025·Nature

VDAC2 loss elicits tumour destruction and inflammation for cancer therapy

Article

Author: Guy, Cliff ; Sun, Xiang ; Sun, Renqiang ; Chapman, Nicole M ; Palacios, Gustavo ; Hu, Haoran ; Meng, Xiaoxi ; Yuan, Sujing ; Gottschalk, Stephen ; Shi, Hao ; Chi, Hongbo ; Zhou, Peipei ; Yang, Xiaoyang ; Kc, Anil ; Rankin, Sherri

Tumour cells often evade immune pressure exerted by CD8⁺ T cells or immunotherapies through mechanisms that are largely unclear^1,2. Here, using complementary in vivo and in vitro CRISPR-Cas9 genetic screens to target metabolic factors, we established voltage-dependent anion channel 2 (VDAC2) as an immune signal-dependent checkpoint that curtails interferon-γ (IFNγ)-mediated tumour destruction and inflammatory reprogramming of the tumour microenvironment. Targeting VDAC2 in tumour cells enabled IFNγ-induced cell death and cGAS-STING activation, and markedly improved anti-tumour effects and immunotherapeutic responses. Using a genome-scale genetic interaction screen, we identified BAK as the mediator of VDAC2-deficiency-induced effects. Mechanistically, IFNγ stimulation increased BIM, BID and BAK expression, with VDAC2 deficiency eliciting uncontrolled IFNγ-induced BAK activation and mitochondrial damage. Consequently, mitochondrial DNA was aberrantly released into the cytosol and triggered robust activation of cGAS-STING signalling and type I IFN response. Importantly, co-deletion of STING signalling components dampened the therapeutic effects of VDAC2 depletion in tumour cells, suggesting that targeting VDAC2 integrates CD8⁺ T cell- and IFNγ-mediated adaptive immunity with a tumour-intrinsic innate immune-like response. Together, our findings reveal VDAC2 as a dual-action target to overcome tumour immune evasion and establish the importance of coordinately destructing and inflaming tumours to enable efficacious cancer immunotherapy.

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BID

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