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single-molecule fluorescence microscopy showed that the microtubule plus-end-associated protein CLIP-170 binds tightly to formins to accelerate actin filament elongation.
We find that LRRK1-mediated phosphorylation of CLIP-170 causes the accumulation of p150(Glued (show DCTN1 ELISA Kits)) (also known as DCTN1 (show DCTN1 ELISA Kits)) a subunit of dynactin (show DCTN1 ELISA Kits), at microtubule plus ends, thereby facilitating the migration of EGFR (show EGFR ELISA Kits)-containing endosomes.
herpesvirus particles are absolutely dependent on CLIP-170-mediated capture to initiate transport in primary human cells.
We show that AMPH-1 (show AMPH ELISA Kits)/BIN1 (show BIN1 ELISA Kits) binds to nesprin and actin, as well as to the microtubule-binding protein CLIP170 in both species. We propose that BIN1 (show BIN1 ELISA Kits) has a direct and evolutionarily conserved role in nuclear positioning, altered in myopathies.
Restin inhibits epithelial-mesenchymal transition and tumor metastasis by controlling the expression of the tumor metastasis suppressor mir (show MLXIP ELISA Kits)-200a/b via association with p73 (show TP73 ELISA Kits).
CLIP-170 tethers kinetochores to microtubule ends against the dynein-mediated poleward force to slide kinetochores along microtubules
A defect in the CLIP1 gene (CLIP-170) can cause autosomal recessive intellectual disability.
Data suggest that CLIP-170 acts as a novel recruiter and spatial regulator of PLK1 (show PLK1 ELISA Kits) at kinetochores during early mitosis, promoting K-fiber stability and chromosome alignment for error-free chromosome segregation.
siRNA-mediated knockdown of the cytoplasmic linker protein compromised the assembly and branching of capillary-like blood vessels and neovascularization in vivo. It was critical for the motility abilities of HUVECs through its actions on cell polarity.
HDAC6 (show HDAC6 ELISA Kits) interacts with cytoplasmic linker protein 170 (CLIP-170) and that these two proteins function together to stimulate the migration of pancreatic cancer cells.
Drosophila CLIP-190 (and potentially also mouse CLIP-170) does not possess a significant role in the axon growth-promoting microtubule machinery.
Cytoplasmic linker protein 170 was ubiquitously expressed in mouse kidney, liver, lung, normal non-atherosclerotic aorta, and atherosclerotic aorta and was partly localized in the vascular endothelium.
Phosphorylation regulates CLIP-170 conformational changes resulting in its autoinhibition.
Restin expressed in vivo suppresses the growth of tumors in nude mice
CLIP170 is a key regulator of microtubule stabilization that is required for enhanced cell spreading and phagocytosis in activated macrophages.
Two +TIPs, CLIP-170 and end-binding protein 3 (EB3 (show MAPRE3 ELISA Kits)), turn over rapidly on MT ends. Diffusion of CLIP-170 and EB3 (show MAPRE3 ELISA Kits) appears to be rate limiting for their binding to MT plus ends.
The protein encoded by this gene links endocytic vesicles to microtubules. This gene is highly expressed in Reed-Sternberg cells of Hodgkin disease. Several transcript variants encoding different isoforms have been found for this gene.
CAP-GLY domain containing linker protein 1
, CAP-Gly domain-containing linker protein 1
, CAP-Gly domain-containing linker protein 1-like
, cytoplasmic linker protein 1
, cytoplasmic linker protein 170 alpha-2
, cytoplasmic linker protein CLIP-170
, restin (Reed-Steinberg cell-expressed intermediate filament-associated protein)
, Clip 170
, Reed-Steinberg cell-espressed intermediate filament-associated protein
, cytoplasmic linker protein 50
, restin (Reed-Steinberg cell-espressed intermediate filament-associated protein)
, cytoplasmic linker protein 170