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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.
upregulation of PRICKLE1 in basal breast cancers, a subtype characterized by high metastatic potential, is associated with poor metastasis-free survival.
Our experimental data demonstrate that high expression of Prickle1 and Vangl2 (Montrer VANGL2 Protéines) reduce the growth of neuroblastoma (Montrer ARHGEF16 Protéines) cells and indicate different roles of PCP (Montrer PRCP Protéines) proteins in tumorigenic cells compared to normal cells.
these findings suggest PRICKLE1 mutations contribute to ASD (Montrer ARSD Protéines) by disrupting the interaction with SYN1 (Montrer SYN1 Protéines) and regulation of synaptic vesicles.
study demonstrates that PRICKLE1 could act as a predisposing factor to human neural tube defects
MINK1 interacts with and phosphorylates PRICKLE1 and PRICKLE2.
Mutations in prickle1 causes seizures.
PRICKLE1 mutations are not a frequent cause of progressive myoclous epilepsies in Southern Italy.
PRICKLE1 and PRICKLE2 mRNAs were expressed together in brain, eye and testis.
appears to serve as a nuclear receptor for REST/NRSF (Montrer REST Protéines), REST4, and possibly other transcription factors
Prickle1 plays a role in positive regulation of differentiation and maturation of oligodendrocytes.
findings argue against the role of Prickle1 in regulating hair cell polarity in the cochlea. Instead, Prickle1 regulates the polarity-related growth of distal and central processes of apical SGNs
Prickle1 is part of a molecular mechanism that regulates facial branchiomotor neurons caudal migration.
these findings suggest PRICKLE1 mutations contribute to ASD (Montrer GUSB Protéines) by disrupting the interaction with SYN1 (Montrer SYN1 Protéines) and regulation of synaptic vesicles.
Data suggest Prickle1 is part of the Wnt5a (Montrer WNT5A Protéines)/PCP (Montrer BMP1 Protéines) signaling, regulating cell polarity and affecting expression of multiple factors to stunt limb growth through altered patterns of gene expression, including the PCP (Montrer BMP1 Protéines) genes Wnt5a (Montrer WNT5A Protéines) and Vangl2 (Montrer VANGL2 Protéines).
Pk1 function in axonal-dendritic development associated with the maturation of CNS neurons.
Prickle1 and Prickle2 promote neurite-like process formation of C1300 cells via the Dvl1 (Montrer DVL1 Protéines)-dependent mechanism
These results suggest that RILP(also known as Prickle) expression and function control REST action more so than does REST expression and is an important regulatory role in cardiomyocyte differentiation.
both Prickle1 and Prickle2 promote neurite-like process formation of C1300 neuroblastoma (Montrer ARHGEF16 Protéines) cells via the Dishevelled (Montrer DVL2 Protéines) dependent pathway
Prickle regulates cell behavior during early Xenopus development; prickle and tes (Montrer TES Protéines) act together to control axial elongation.
This gene encodes a nuclear receptor that may be a negative regulator of the Wnt/beta-catenin signaling pathway. The encoded protein localizes to the nuclear membrane and has been implicated in the nuclear trafficking of the transcription repressors REST/NRSF and REST4. Mutations in this gene have been linked to progressive myoclonus epilepsy. Alternate splicing results in multiple transcript variants. A pseudogene of this gene is found on chromosome 3.
REST (RE-1 silencing transcription factor)/NRSF (neuron-restrictive silencer factor)-interacting LIM domain protein
, REST/NRSF-interacting LIM domain protein 1
, prickle-like 1
, prickle-like protein 1
, prickle like 1
, LIM protein prickle
, prickle-like protein 1-A
, prickle homolog 1