BOK-MCL1 transmembrane interactions: a challenging target for cancer therapy.
Mónica SanchoMar OrzáezPublished in: Molecular & cellular oncology (2021)
Myeloid cell leukemia 1 (MCL1) gene amplification occurs in a wide range of human cancers and protein overexpression associates with malignant cell growth and evasion of apoptosis. We recently reported that disrupting the interaction between the transmembrane domains of MCL1 and BCL-2 related ovarian killer (BOK) induces cell death, thereby suggesting a new target site for anti-tumorigenic strategies.
Keyphrases
- cell death
- cancer therapy
- cell cycle arrest
- acute myeloid leukemia
- bone marrow
- endothelial cells
- drug delivery
- oxidative stress
- single cell
- cell proliferation
- endoplasmic reticulum stress
- dendritic cells
- cell therapy
- genome wide
- transcription factor
- induced pluripotent stem cells
- nucleic acid
- gene expression
- pluripotent stem cells
- binding protein
- young adults
- amino acid
- protein protein
- immune response
- dna methylation
- mesenchymal stem cells
- drug induced