ArticleMolecular carcinogenesis2019
Tumor suppressor KIF1Bβ regulates mitochondrial apoptosis in collaboration with YME1L1.
Article in Molecular carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- YME1L1 degradation by TRIM21 inhibits bladder cancer proliferation, metastasis, and mitochondrial function.Oncogene · 2026Article
- Identification of prognostic signatures in pheochromocytomas and paragangliomas based on mitochondrial autophagy and ferroptosis in TCGA and GEO datasets.Discover oncology · 2026Article
- Article
- Targeted Sirtuin 3 Activation by Biomimetic Black Phosphorus Nanosheets Mitigates Sepsis-Induced Acute Kidney Injury through Yeast Mitochondrial Escape 1-Like 1 Deacetylation.Biomaterials research · 2026Article
- KIF1B Regulates NLRP3-Mediated Pyroptosis in Asthma Progression.Journal of cellular and molecular medicine · 2025Article
- An ultra-rare missense variant in the KIF1B gene linked to autoinflammatory Menière's disease.NPJ genomic medicine · 2025Article
- SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification and Experimental Validation of Biomarkers Associated With Mitochondria and Macrophage Polarization in Sepsis.Emergency medicine international · 2025Article
- CX‑5461 potentiates imatinib‑induced apoptosis in K562 cells by stimulatingExperimental and therapeutic medicine · 2024Article
- Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling.Chemical science · 2023Article
- Proteomic analysis for the effects of non-saponin fraction with rich polysaccharide from Korean Red Ginseng on Alzheimer's disease in a mouse model.Journal of ginseng research · 2023Article
- Circ_0049472 regulates the damage of Aβ-induced SK-N-SH and CHP-212 cells by mediating the miR-107/KIF1B axis.Experimental brain research · 2022Article
- Revealing potential diagnostic gene biomarkers of septic shock based on machine learning analysis.BMC infectious diseases · 2022Article
- Analysis of signature genes and association with immune cells infiltration in pediatric septic shock.Frontiers in immunology · 2022Article
- Haploinsufficient tumor suppressor PRP4K is negatively regulated during epithelial-to-mesenchymal transition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- RevisitingMicroorganisms · 2021Article
- Motor proteins at the mitochondria-cytoskeleton interface.Journal of cell science · 2021Review
- What Have We Learned from Molecular Biology of Paragangliomas and Pheochromocytomas?Endocrine pathology · 2021Review
- "The Loss of Golden Touch": Mitochondria-Organelle Interactions, Metabolism, and Cancer.Cells · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KIF1Bβ, a member of the kinesin superfamily of motor proteins, is a haploinsufficient tumor suppressor mapped to chromosome 1p36.2, which is frequently deleted in neural crest-derived tumors, including neuroblastoma and pheochromocytoma. While KIF1Bβ acts downstream of the nerve growth factor (NGF) pathway to induce apoptosis, further molecular functions of this gene product have largely been unexplored. In this study, we report that KIF1Bβ destabilizes the morphological structure of mitochondria, which is critical for cell survival and apoptosis. We identified YME1L1, a mitochondrial metalloprotease responsible for the cleavage of the mitochondrial GTPase OPA1, as a physical interacting partner of KIF1Bβ. KIF1Bβ interacted with YME1L1 through its death-inducing region, as initiated the protease activity of YME1L1 to cleave the long forms of OPA1, resulting in mitochondrial fragmentation. Overexpression of YME1L1 promoted apoptosis, while knockdown of YME1L1 promoted cell growth. High YME1L1 expression was significantly associated with a better prognosis in neuroblastoma. Furthermore, in NGF-deprived PC12 cells, KIF1Bβ and YME1L1 were upregulated, accompanied by mitochondrial fragmentation and apoptotic cell death. Small interfering RNA-mediated knockdown of either protein alone, however, remarkably inhibited the NGF depletion-induced apoptosis. Our findings indicate that tumor suppressor KIF1Bβ plays an important role in intrinsic mitochondria-mediated apoptosis through the regulation of structural and functional dynamics of mitochondria in collaboration with YME1L1. Dysfunction of the KIF1Bβ/YME1L1/OPA1 mechanism may be involved in malignant biological features of neural crest-derived tumors as well as the initiation and progression of neurodegenerative diseases.
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