BIK Antibodies

Background

The BCL2-interacting killer protein encoded by the BIK gene is a pro-apoptotic protein, mainly located on the outer mitochondrial membrane, and belongs to the BCL-2 protein family containing only the BH3 domain. This protein plays a key role in regulating programmed cell death by interacting with anti-apoptotic proteins such as BCL-2 and BCL-XL to activate the apoptotic pathway. The abnormal expression of the BIK gene is closely related to the occurrence and development of various cancers, and its functional research is helpful in revealing the escape mechanism of tumor cells. Since its discovery in the 1990s, BIK has continuously attracted attention due to its fundamental position in the apoptotic signaling pathway, providing an important perspective for understanding the maintenance of cell homeostasis, the pathological mechanisms of cancer, and the development of potential therapeutic targets.

Structure Function Application Advantage Our Products

Structure of BIK

BIK protein is a pro-apoptotic protein with a molecular weight of approximately 21 kDa. Its precise molecular weight varies slightly among different species, mainly due to amino acid sequence variations near the BH3 domain.

Species	Human	Mouse	Rat
Molecular Weight (kDa)	21.0	20.8	20.9
Primary Structural Differences	Containing 192 amino acids, the typical structure of BH3 domain	BH3 domain structure highly conservative, n-terminal sequence is slightly different	With the human BIK high homology, similar functions

The BIK protein is composed of approximately 160 to 200 amino acids, and its primary structure contains a key BH3 domain, which is the core motif for its interaction with anti-apoptotic proteins (such as BCL-2 and BCL-XL) and the execution of pro-apoptotic functions. The overall conformation of BIK is relatively loose and lacks a typical spherical structure. Its C-terminal transmembrane domain is responsible for anchoring it to the outer mitochondrial membrane. The BH3 domain forms an amphiphilic α -helix, and its hydrophobic surface directly binds to the hydrophobic groove of the anti-apoptotic protein, thereby relieving its inhibition of apoptosis and triggering programmed cell death.

Fig. 1:BIK upregulation causes sublethal apoptosis and cancer aggression. Fig. 1 BIK upregulation causes sublethal apoptosis and cancer aggression.¹

Key structural properties of BIK:

Contains the key BH3 amphipathic α-helix domain
With C end across membrane anchoring area, located in the mitochondrial membrane
The BH3 domain binds directly to hydrophobic grooves of anti-apoptotic proteins such as BCL-2
The overall structure is relatively loose and lacks a typical spherical folded conformation

Functions of BIK

The core function of the BIK gene is to act as a key regulatory factor for apoptosis. However, it is also involved in a variety of cellular processes, including responses to cellular stress signals and regulation of tumorigenesis.

Function	Description
Induce apoptosis	The BIK protein binds to anti-apoptotic proteins (such as BCL-2/BCL-XL) through its BH3 domain, relieving their inhibition of apoptosis and thereby initiating programmed cell death.
Response to stress signals	Under intracellular stress (such as endoplasmic reticulum stress and DNA damage), the expression of BIK is upregulated, thereby promoting the clearance of damaged cells.
Tumor suppression	By inducing apoptosis of precancerous lesions or tumor cells, BIK plays an important role in tumor suppression, and its dysfunction is related to cancer development.
Autophagy regulation	BIK has been found to interact with autophagy pathway proteins and participate in regulating autophagic cell death under specific circumstances.
Developmental regulation	During the process of tissue development and homeostasis maintenance, BIK participates in eliminating redundant or abnormal cells to ensure the normal morphology and function of organs.

Unlike the extensive activation of multi-domain pro-apoptotic proteins (such as BAX and BAK), BIK, as a "sensitizer" or "direct activator", its activity is highly dependent on the specific interaction of the BH3 domain, which reflects its precise regulatory role in the apoptotic signaling network.

Applications of BIK and BIK Antibody in Literature

1. Soni, Sourabh, et al. "BIK polymorphism and proteasome regulation unveil host risk factor for severe influenza." Proceedings of the National Academy of Sciences 122.28 (2025): e2424367122. https://doi.org/10.1073/pnas.2424367122

This article found that the host gene BIK is a key factor for the replication of influenza A virus. Viral nucleoproteins increase the level of BIK by inhibiting the β5 subunit of the proteasome, thereby promoting viral replication. BIK gene variation (rs738276) affects the viral replication ability in human airway epithelial cells and is associated with the severity of influenza. Targeting the BIK-β5 axis may become a potential therapeutic strategy.

2. Mebratu, Yohannes A., et al. "Bik reduces hyperplastic cells by increasing Bak and activating DAPk1 to juxtapose ER and mitochondria." Nature Communications 8.1 (2017): 803. https://doi.org/10.1038/s41467-017-00975-w

This study revealed that BIK dissociates the Bak/Bcl-2 complex through its BH3 domain and forms complexes with proteins such as DAPk1, promoting the release of endoplasmic reticulum calcium into mitochondria, thereby inducing apoptosis and reducing proliferative epithelial cells. The BIK-derived peptide segments designed based on this mechanism effectively alleviated airway mucus hypersecretion in experiments, demonstrating therapeutic potential.

3. Soni, Sourabh, et al. "Independent role of caspases and Bik in augmenting influenza A virus replication in airway epithelial cells and mice." Virology journal 20.1 (2023): 78. https://doi.org/10.1186/s12985-023-02027-w

This study confirmed that in the replication of influenza virus, BIK mainly functions by activating Caspase-3 and other caspases and downstream PARP1, but the role of BIK is not limited to this. The absence of BIK can lead to a significant decrease in viral titer, while the use of broad-spectrum Caspase inhibitors can further inhibit viral replication, suggesting that BIK also has a virus-promoting mechanism that is independent of Caspase/PARP1. Targeting this pathway may become a potential therapeutic strategy.

4. Pandya, Vrajesh, et al. "BIK drives an aggressive breast cancer phenotype through sublethal apoptosis and predicts poor prognosis of ER-positive breast cancer." Cell Death & Disease 11.6 (2020): 448. https://doi.org/10.1038/s41419-020-2654-2

This study reveals that in estrogen receptor-positive breast cancer, the highly expressed BIK protein can induce "incomplete apoptosis" : that is, initiating the apoptosis program without causing cell death, but instead causing DNA damage. Surviving cells acquire the characteristics and invasiveness of stem cells, leading to tumor recurrence. Therefore, BIK can be used as a biomarker for predicting clinical recurrence in such patients.

5. Mebratu, Yohannes A., et al. "Bik promotes proteasomal degradation to control low-grade inflammation." The Journal of Clinical Investigation 134.4 (2024). https://doi.org/10.1172/JCI177753

This study reveals that BIK deficiency can induce spontaneous emphysema in female mice, indicating that it plays a key role in inhibiting persistent low-grade airway inflammation associated with chronic obstructive pulmonary disease (COPD) in women. This discovery provides a new mechanism for understanding the gender differences in the prevalence and clinical manifestations of COPD, emphasizing the importance of conducting specific research and treatment for women.

Creative Biolabs: BIK Antibodies for Research

Creative Biolabs specializes in the production of high-quality BIK antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

Custom BIK Antibody Development: Tailor-made solutions to meet specific research requirements.
Bulk Production: Large-scale antibody manufacturing for industry partners.
Technical Support: Expert consultation for protocol optimization and troubleshooting.
Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our BIK antibodies, custom preparations, or technical support, contact us at email.

Reference

Pandya, Vrajesh, et al. "BIK drives an aggressive breast cancer phenotype through sublethal apoptosis and predicts poor prognosis of ER-positive breast cancer." Cell Death & Disease 11.6 (2020): 448. https://doi.org/10.1038/s41419-020-2654-2