Authors
Lawrence Tucker, Anca-Narcisa Neagu, Petra Kraus, Costel C Darie
Published in
Advances in experimental medicine and biology. Volume 1359. Pages 89-102.
Abstract
Jumping Translocation Breakpoint (JTB) is a highly conserved protein expressed across multiple tissues and organs, yet its expression levels vary depending on developmental stage, tissue type, and disease state. Organ-level studies indicate that JTB is upregulated in regions of rapid growth and regeneration, suggesting a role in proliferation and tissue development, and hinting at a connection to neural crest (NC) cells and epithelial-mesenchymal transition (EMT) events relevant to cancer biology. At the subcellular level, JTB localization remains debated: some evidence links it to mitochondria, affecting membrane potential and morphology, while other studies indicate transient association with the Chromosomal Passenger Complex (CPC) during mitosis, implicating it in cell cycle regulation. JTB exists in multiple isoforms, including variants with cleaved signaling or transmembrane regions, which may modulate its function and localization. Resolving discrepancies in subcellular localization and understanding isoform-specific roles are critical for elucidating JTB's full biological function and its potential relevance in developmental and cancer-related processes.
PMID:
42907625
Bibliographic data and abstract were imported from PubMed on 23 Oct 2026.
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