ArticlePloS one2013
MCL-1ES induces MCL-1L-dependent BAX- and BAK-independent mitochondrial apoptosis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Pharmacological blockade of rho kinase enhances venetoclax responses in translational models of acute myeloid leukemia.Haematologica · 2026Article
- SRSF1/Mcl-1 Axis Drives Apoptosis Evasion and Shapes the Immune Microenvironment to Promote Gastric Cancer Progression.Human mutation · 2026Article
- The chloroform fraction of Dracontium spruceanum modulates gene expression in gastric cancer stem cells.Scientific reports · 2025Article
- Understanding MCL1: from cellular function and regulation to pharmacological inhibition.The FEBS journal · 2022Review
- The Ethyl Acetate Fraction of Marine Sponge Stylissa carteri Induces Breast Cancer Cell Death via Upregulation of Mcl-1S: an In vitro Study.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Guanylate-binding proteins induce apoptosis of leukemia cells by regulating MCL-1 and BAK.Oncogenesis · 2021Article
- Targeting MCL-1 in cancer: current status and perspectives.Journal of hematology & oncology · 2021Review
- Review
- BCL-2 family isoforms in apoptosis and cancer.Cell death & disease · 2019Review
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
- Inhibition of the oncogenic fusion protein EWS-FLI1 causes GScience signaling · 2017Article
- MCL-1 is modulated in Crohn's disease fibrosis by miR-29b via IL-6 and IL-8.Cell and tissue research · 2017Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MCL-1 (myeloid cell leukemia-1), a member of the BCL-2 family, has three splicing variants, antiapoptotic MCL-1L, proapoptotic MCL-1S, and MCL-1ES. We previously reported cloning MCL-1ES and characterizing it as an apoptotic molecule. Here, we investigated the molecular mechanism by which MCL-1ES promotes cell death. MCL-1ES was distinct from other proapoptotic BCL-2 members that induce apoptosis by promoting BAX or BAK oligomerization, leading to mitochondrial outer membrane permeabilization (MOMP), in that MCL-1ES promoted mitochondrial apoptosis independently of both BAX and BAK. Instead, MCL-1L was crucial for the apoptotic activity of MCL-1ES by facilitating its proper localization to the mitochondria. MCL-1ES did not interact with any BCL-2 family proteins except for MCL-1L, and antiapoptotic BCL-2 members failed to inhibit apoptosis induced by MCL-1ES. The BCL-2 homology 3 (BH3) domain of MCL-1ES was critical for both MCL-1ES association with MCL-1L and apoptotic activity. MCL-1ES formed mitochondrial oligomers, and this process was followed by MOMP and cytochrome c release in a MCL-1L-dependent manner. These findings indicate that MCL-1ES, as a distinct proapoptotic BCL-2 family protein, may be useful for intervening in diseases that involve uncontrolled MCL-1L.
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