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Pleckstrin homology domain-containing family O member 1 (PLEKHO1, also known as CKIP-1)
- Target
- PLEKHO1, also known as CKIP-1
- Molecular classification
- Adapter protein (cell signaling), Cytoskeletal regulatory protein, Pleckstrin homology domain-containing protein
01
Overview
Pleckstrin homology domain-containing family O member 1 (PLEKHO1, also known as CKIP-1) is a cytoplasmic adapter protein encoded by the PLEKHO1 gene in humans. It contains a pleckstrin homology (PH) domain, which is critical for membrane localization and interaction with phosphoinositide lipids, actin capping protein, casein kinase 2 (CK2), and other partners. PLEKHO1 orchestrates molecular processes including actin cytoskeleton regulation, cell morphology, myoblast fusion/differentiation, and apoptosis. It acts as an inhibitor of tumor cell growth by impeding AKT-mediated cell survival signaling and may play a role in muscle differentiation. Its molecular actions are relevant in contexts including cancer, cell motility/invasion, and muscle or bone development
- Other names
- PLEKHO1CKIP-1OC120CKIP1JBPPleckstrin homology domain containing O1
02
Mechanism of action
No direct drugs; however, modulation of its interactions (for instance, by targeting CK2 or AKT pathways, or influencing PI3K signaling) could affect cell proliferation, apoptosis, and cytoskeleton integrity.
03
Biological functions
Regulation of actin cytoskeletonCell morphology modulationMyoblast fusion and migrationCell differentiationPromotion of apoptosis (including TNF-induced)Inhibition of tumor cell growth via AKT pathway inhibitionMuscle differentiationRegulation of AP-1 activity
04
Disease associations
Cancer (due to inhibition of AKT-mediated cell survival and tumor inhibition)Potential muscle and bone phenotype roles (because of myoblast fusion/differentiation effects)Other (related to apoptosis, cell motility, and differentiation)
05
Safety considerations
No documented safety concerns or therapeutic challenges associated with targeting PLEKHO1 directly in the current literature. Risks might be inferred through effects on actin cytoskeletal integrity or apoptosis.
06
Interacting drugs
There are currently no well-established direct pharmacologic inhibitors or activators of PLEKHO1 in clinical use found in the search results. Experimental modulation would occur through upstream pathways such as CK2, AKT, and PI3K.
07
Biomarkers
No clinical biomarkers directly associated with PLEKHO1 for patient selection or efficacy noted in the available sources.
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