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MOB kinase activator 1B (MOB1B)
- Target
- MOB1B
- Molecular classification
- Kinase activator, Signal transduction adapter protein, Signaling scaffold, Other (member of the "MOB kinase activators" family)
01
Overview
MOB kinase activator 1B (MOB1B) is a highly conserved signaling protein that functions as a core component and activator within the Hippo pathway—a critical regulator of organ size, cell proliferation, stem cell self-renewal, and tumor suppression[1][5]. MOB1B acts by binding and activating LATS1/2 kinases and orchestrates downstream phosphorylation events that restrain the activity of growth-promoting factors such as YAP/TAZ. It is regulated through phosphorylation (notably at Thr12 and Thr35), which relieves its autoinhibited state and allows it to interact with kinases in the Hippo pathway[1][2][4][5]. MOB1B is essential for proper cytokinesis, ensuring successful cell division and maintenance of genomic stability, and its loss or downregulation is linked to cancer development and tissue homeostasis breakdown, particularly in epithelia[3][5]. No drugs directly target MOB1B, but its central role in growth control and tumor suppression makes it an intensively studied molecule in cancer biology.
- Other names
- MOBKL1AMATS2MOB4AMps one binder kinase activator-like 1AMob1AMob1Bmob1 homolog 1Amob1Amob1BMob4A proteinMOB1Mps One Binder homolog BMOB1 Mps One Binder homolog B
02
Biological functions
Regulation of Hippo signaling pathwayActivation of LATS1 and LATS2 kinasesRegulation of cell proliferation and organ sizeTumor suppressionRegulation of cell cycle and cytokinesisMaintenance of tissue homeostasisCell death, apoptosisRegulation of stem cell compartment and differentiation in epithelia
03
Disease associations
Cancer (especially as a tumor suppressor; downregulation associated with enhanced proliferation, invasion, and migration)Intestinal epithelial degenerationObesity-related endometrial cancerOther (potential implication in tissue regeneration and failure of cell division)
04
Safety considerations
Loss of MOB1B activity can result in hyperproliferation, impaired cellular differentiation, and disruption of critical signaling networks, which may contribute to oncogenesis or tissue degeneration if targeted inappropriately
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