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Data suggest that Nrx-1 plays critical roles in regulating synaptic terminal clustering and release of synaptic vesicles of the neuromuscular junction; Nrx-1 controls terminal clustering and release of synaptic vesicles by stimulating presynaptic actin cytoskeleton assembly; Nrx-1 functions via Scribble and Pixie to activate Rac1. (Nrx-1 = neurexin-1; Rac1 = GTP-binding protein Rac1)
the simultaneous loss of the asymmetric cell division regulators Canoe (afadin (show MLLT4 ELISA Kits) in mammals) and Scribble in neuroblast clones leads to tumor-like overgrowth through both a severe disruption of the asymmetric cell division process and canoe loss-mediated Ras-PI3K-Akt (show AKT1 ELISA Kits) activation
the effects of loss of scrib and the modification of these effects via cooperative interactions that enhance the overall tumorigenic potential of scrib deficient cells, is reported.
Knocking down scribble expression in either Mushroom body neurons or Dopaminergic neurons impairs normal memory loss.
Our data reveal that the basolateral determinant Scribbled (Scrib) is required for PCV formation through optimizing BMP (show TGFb ELISA Kits) signaling. Scrib regulates BMP (show TGFb ELISA Kits)-type I receptor Thickveins (Tkv) localization at the basolateral region of PCV cells and subsequently facilitates Tkv internalization to Rab5 (show RAB5A ELISA Kits) endosomes, where Tkv is active
Scrib module regulates epithelial polarity by influencing endocytic itineraries of Crumbs and other retromer-dependent cargo.
Loss of scrib, dlg (show DLG4 ELISA Kits) and lgl had no effect on gonad formation, but Dlg (show DLG4 ELISA Kits) and Scrib in the gonadal mesoderm acted critically in the somatic wrapping of the pole cells and the internal structure of the Drosophila embryonic gonads.
Drosophila scrib acts downstream of the Fat (Ft) receptor, and requires Hippo signaling for its growth regulatory functions.
Loss of Scrib promotes Yorkie (show YAP1 ELISA Kits)/Scalloped-dependent epithelial tissue overgrowth, and this is also important for driving cooperative tumor overgrowth with oncogenic Ras-Raf (show RAF1 ELISA Kits) signaling.
Data show that mutations causing the loss of Salvador (Sav (show SAV1 ELISA Kits)) or Scribble (Scrib) or activation of Ras transform normal stem cells into cancer stem cells through a multistep process in the adult Drosophila Malpighian tubules.
SCRIB is a positive regulator of mammary epithelial cell proliferation during pregnancy.
Suggest a role for Plexin-B1 (show PLXNB1 ELISA Kits) as a ligand and Sema4A (show Sema4a ELISA Kits) as a receptor and characterize a reverse signaling pathway downstream of Sema4A (show Sema4a ELISA Kits) regulating cell migration via Scrib.
SCRIB uncouples reactive oxygen species-dependent bacterial killing activity from M1 polarization and inflammatory functions of macrophages
we provide genetic evidence of a unique link between skin carcinogenesis and loss of the epithelial polarity regulator Scrib, emphasizing that Scrib exerts a wide-spread tumor suppressive function in epithelia.
The polarity protein Scribble regulates myelination and remyelination in the central nervous system.
Scrib is a regulator of tissue stem cells, controlling population expansion and self-renewal with Scrib expression dynamics directing satellite cell fate.
Scrib is a novel proinflammatory regulator in endothelial cells, which maintains the protein expression of GATA-like protein-1.
The Scrib-Rac1 interaction plays a crucial role in the organization of developing cardiomyocytes and formation of the ventricular myocardium.
We show that loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors
findings, based on a definitive genetic mouse model provide fundamental insights into mammary duct maturation and homeostasis and reveal that Scrib loss activates a MAPK (show MAPK1 ELISA Kits)/Fra1 (show FOSL1 ELISA Kits) pathway that alters mammary progenitor activity
Results demonstrate that anterior guidance decisions by commissural primary ascending (CoPA (show COPA ELISA Kits)) axons are dependent on the function of planar cell polarity genes Fzd3a, Vangl2 (show VANGL2 ELISA Kits) and Scribble both prior to and after midline crossing; experiments establish CoPA (show COPA ELISA Kits) axons as a model system to investigate the mechanism of planar cell polarity signaling in commissural axon guidance.
Zygotic expression of Scribble1 (scrb1) is required for migration of the nVII motor neurons mainly in a non cell-autonomous manner, while maternal expression is required for convergent extension movements during gastrulation.
Suppression of scrib and puf60 in zebrafish (show PUF60 ELISA Kits)leads to reduction in body length, small head size, and craniofacial defects.
It was found that Scribble is required for oriented cell division and that its function in this process is independent of canonical apicobasal and planar polarity pathways.
Lpp interacts with the PCP (show PRCP ELISA Kits) protein Scrib in zebrafish, and that Lpp and Scrib cooperate for the mediation of convergence and extension.
Scribble is a candidate link between Fat and the Hippo signaling cascade in vertebrates
inhibiting acyl thioesterase (show FASN ELISA Kits) 2 restores balance to the Scrib palmitoylation cycle, promoting membrane re-localization and growth attenuation
sequencing analysis of SCRIB1 in 473 NTD patients led to the identification of 5 rare heterozygous missense mutations that were predicted to be pathogenic. Two of these mutations, p.Gly263Ser and p.Gln808His, and 2 mouse NTD mutations, p.Ile285Lys and p.Glu814Gly, affected Scrib1 membrane localization and its modulating role of Par-3 (show F2RL2 ELISA Kits) and Vangl1 (show Vangl1 ELISA Kits) localization.
a new function for Scribble in Rho regulation that entails positioning of DLC3 (show STARD8 ELISA Kits) GAP activity at cell junctions in polarized epithelial cells, is reported.
Low Scribble expression in the primary breast tumor was correlated to prognosis in estrogen receptor (show ESR1 ELISA Kits)-positive breast cancer patients.
The Palmitoylation-deficient mutants of SCRIB were mislocalized, leading to disruption of cell polarity and loss of their tumor-suppressive activities to oncogenic YAP (show YAP1 ELISA Kits), MAPK (show MAPK1 ELISA Kits) and PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) pathways.
Data show hepatitis C virus (HCV) nonstructural protein 4B (NS4B) PDZ (show INADL ELISA Kits)-binding motif (PBM) promotes the colony formation of hepatoma cells by degrading human Scribble protein.
the inclusion/exclusion of specific SCRIB exons is a mechanistic hallmark of breast cancer, which could potentially be exploited to develop more efficient diagnostics and therapies.
loss of Scribble-induced HuR (show ELAVL1 ELISA Kits) translocation mediates the accumulation of Snail (show SNAI1 ELISA Kits) via activation of the p38 MAPK (show MAPK14 ELISA Kits) pathway.
This gene encodes a protein that was identified as being similar to the Drosophila scribble protein. The mammalian protein is involved in tumor suppression pathways. As a scaffold protein involved in cell polarization processes, this protein binds to many other proteins. The encoded protein binds to papillomavirus E6 protein via its PDZ domain and the C-terminus of E6. Two alternatively spliced transcript variants that encode different protein isoforms have been found for this gene.
, immune response deficient 15
, lethal (3) c00119
, smell impaired 97B
, PDZ-domain protein scribble
, protein scribble homolog
, scribble homolog 1
, scribbled homolog