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data reveal that CLASP2 is an essential Reelin (show RELN ELISA Kits) effector orchestrating cytoskeleton dynamics during brain development.
These findings reveal a new role for Clasp2 in governing keratinocyte undifferentiated features.
A transport system, organized by agrin (show AGRN ELISA Kits) through PI3 kinase (show PIK3CA ELISA Kits), GSK3beta (show GSK3b ELISA Kits), CLASP2, and LL5beta, for precise delivery of acetylcholine receptor (show CHRNB1 ELISA Kits) vesicles from subsynaptic nuclei to overlying synaptic membrane was identified at neuromuscular junction membrane.
the functional relationship between Abl (show ABL1 ELISA Kits) and CLASP2 is conserved and provides a means to control the CLASP2 association with the cytoskeleton.
The MT plus end-binding protein CLASP2 localizes to adherens junctions (AJs) via direct interaction with p120-catenin (p120 (show CTNND1 ELISA Kits)) in primary basal mouse keratinocytes.
CLASP2 is required for the proper attachment of fibroblasts, HSC (show FUT1 ELISA Kits)-enriched cells, and platelets, indicating a general role for this protein in cell attachment.
CLASP2 directs the delivery of GLUT4 (show SLC2A4 ELISA Kits) to cell cortex landing zones important for insulin (show INS ELISA Kits) action
Short-hairpin RNA-mediated CLASP2 knockdown in mouse neurons decreases axon & dendritic length. It is involved in cytoskeleton-related neuronal polarity & interplay between microtubule stabilization & synapse formation & activity.
the cascade linking agrin (show AGRN ELISA Kits) to CLASP2-mediated microtubule capturing at the synaptic membrane is essential for the maintenance of a normal neuromuscular phenotype
Regional immobilization of CLASP2 allows MT stabilization and promotes directionally persistent motility in fibroblasts.
Prickle1 localized to the membrane through its farnesyl moiety, and the membrane localization was necessary for Prickle1 to regulate migration, to bind to CLASPs and LL5beta, and to promote microtubule targeting of focal adhesions.
this study shows that GSK3 (show GSK3b ELISA Kits)-mediated phosphorylation of CLASP2alpha largely abolishes CLASP2alpha-microtubule association in metaphase thus contributing to correct chromosome dynamics
PAR3 (show F2RL2 ELISA Kits) and aPKC control the organization of the Golgi through CLASP2 phosphorylation.
GSK3B (show GSK3b ELISA Kits)-dependent phosphorylation and the level of CLASP2 play a role in the maintenance of acetylcholine receptor (show CHRNA1 ELISA Kits) cluster size through the regulated capture and release of microtubule plus-ends.
Propose that CLASPs couple microtubule organization, vesicle transport and cell interactions with the ECM (show MMRN1 ELISA Kits), establishing a local secretion pathway that facilitates focal adhesion turnover by severing cell-matrix connections.
Interstitial deletion of 3p22.3p22.2 encompassing ARPP21 (show ARPP21 ELISA Kits) and CLASP2 is a potential pathogenic factor for a syndromic form of intellectual disability.
Results suggest a previously unidentified role for the scaffolding protein 4.1R (show EPB41 ELISA Kits) in locally controlling CLASP2 behavior, CLASP2 cortical platform turnover and GSK3 (show GSK3b ELISA Kits) activity, enabling correct MT organization and dynamics essential for cell polarity.
The epiblast epithelial status was maintained by anchoring microtubules to the basal cortex via CLIP2, a microtubule plus-end tracking protein, and Dystroglycan, a transmembrane protein that bridges the cytoskeleton and basement membrane (BM).
Overexpression of human CLASP2 in mouse neurons caused the formation of multiple axons, enhanced dendritic branching, & Golgi condensation. These morphogenetic changes led to significant functional alterations in synaptic transmission.
Microtubule plus-end tracking protein that promotes the stabilization of dynamic microtubules. May be involved in the nucleation of noncentrosomal microtubules originating from the trans-Golgi network (TGN). Required for the polarization of the cytoplasmic microtubule arrays in migrating cells towards the leading edge of the cell. Also performs a similar stabilizing function at the kinetochore which is essential for the bipolar alignment of chromosomes on the mitotic spindle (By similarity).
CLIP-associating protein 2
, cytoplasmic linker-associated protein 2
, cytoplasmic linker associated protein 2
, CLIP-associating protein CLASP2
, multiple asters (Mast)-like homolog 2
, protein Orbit homolog 2
, CLIP associating protein 2