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The reduced expression of Parkin and HtrA2 interpret defective mitophagy leading to clustering of fragmented mitochondria and apoptotic inhibition in scrib knockdown tumors.
a Studies indicate a role for Scribble protein during eye and wing development [Review]
findings reveal that Scrib's PDZ1 domain functions in the interaction with Gukh and that the Scrib-Gukh interaction has a key role in epithelial tissue development in Drosophila
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 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 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 signaling. Scrib regulates BMP-type I receptor Thickveins (Tkv) localization at the basolateral region of PCV cells and subsequently facilitates Tkv internalization to Rab5 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 and lgl had no effect on gonad formation, but Dlg 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/Scalloped-dependent epithelial tissue overgrowth, and this is also important for driving cooperative tumor overgrowth with oncogenic Ras-Raf signaling.
Data show that mutations causing the loss of Salvador (Sav) 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.
interaction between Ras(V12) and scrib(-) clones involves JNK signalling propagation and JNK-induced upregulation of JAK/STAT-activating cytokines, a compensatory growth mechanism for tissue homeostasis
These results demonstrate distinct aPKC and JNK-dependent pathways through which loss of Scrib promotes tumourigenesis in Drosophila.
Study provide evidence that scrib and dlg function differentially in anterior and posterior patterning of the follicular epithelium at oogenesis. Further genetic analysis indicates that scrib and dlg act in a common pathway to regulate PFC fate induction.
conclude that Dlg/Scrib/Lgl are important in regulating cortical polarity, cell size asymmetry and mitotic spindle asymmetry in Drosophila neuroblasts
Scrib is essential for olfactory behavior in D. melanogaster.
Scribble deficiency reduces surface expression of Epo receptor but selectively retains survival signaling via Akt.
Scribdeficient hematopoietic stem cells reveal impaired migratory capacity.
Results identify a key planar cell polarity (PCP) protein, Scrib, as one of the fundamental scaffold proteins that enable hippocampal glutamatergic synapses to mature and to express bidirectional plasticity required for memory formation. Study offers a unique insight into the mechanism by which the PCP protein Scrib can regulate memory formation at postnatal stages.
In the Scrib mutant, despite severe neural tube defects, epF and preBotC neurons settled at their expected hindbrain positions. Furthermore, both networks remained capable of generating rhythmically organized, respiratory-related activities and exhibited normal sensitivity to pharmacological agents known to modify respiratory circuit function.
SCRIB is a positive regulator of mammary epithelial cell proliferation during pregnancy.
Suggest a role for Plexin-B1 as a ligand and Sema4A as a receptor and characterize a reverse signaling pathway downstream of Sema4A 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/Fra1 pathway that alters mammary progenitor activity
The Scribble knockout fetus exhibits exomphalos (intact and ruptured), in contrast to the original published phenotype of gastroschisis.
Scrib is required to maintain epithelial identity and that loss of Scrib can culminate in EMT, mediated, at least in part, through TGFbeta signaling.
B cell differentiation does not require polarity proteins of the Scribble complex, and the findings do not support a role for asymmetric cell division in B cell activation and differentiation.
Scrib is required for normal lung epithelial organisation and lumen morphogenesis by maintaining cell-cell contacts.
while Scribble seems to be important for general epithelial cell and pronephros development, it appears to be dispensable for podocyte function and development
Mutation in the planar cell polarity gene, Scrib, and a mutation in caspase-3 gene have the most profound effect in controlling neural development.
Results demonstrate that anterior guidance decisions by commissural primary ascending (CoPA) axons are dependent on the function of planar cell polarity genes Fzd3a, Vangl2 and Scribble both prior to and after midline crossing; experiments establish CoPA 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 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 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
Perturbation of hepatocellular polarity due to overexpression and cytoplasmic enrichment of Scrib supports tumor initiation and hepatocellular carcinoma cell dissemination through specific molecular mechanisms
Data suggest that millisecond dynamic changes in PDZ1 domain conformation are responsible for higher affinity of scribble PDZ1 for phosphorylated ligands; oligopeptide fragments of RPS6KA2 and MCC were used as ligands in these nuclear magnetic resonance chemical shift experiments. (RPS6KA2 = ribosomal protein S6 kinase 2; MCC = mutated in colorectal cancer protein)
Scrib inhibits liver cancer cell proliferation by suppressing the expression of three oncogenes, Yap1, c-Myc and cyclin D1, thereby functioning as a tumor suppressor in liver cancer.
In this study the authors show that human Scrib expression is required for maintaining high levels of human papillomavirus type 18 E6 protein in HeLa cells.
Data suggest that Scribble PDZ-domain-1 and PDZ-domain-3 are major domains that interact with beta-PIX and exhibit distinct binding hierarchy in interactions between individual Scribble PDZ domains and beta-PIX. (Scribble = scribbled planar cell polarity protein; beta-PIX = Rho guanine nucleotide exchange factor 7)
inhibiting acyl thioesterase 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 and Vangl1 localization.
a new function for Scribble in Rho regulation that entails positioning of DLC3 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-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, MAPK and PI3K/AKT pathways.
Data show hepatitis C virus (HCV) nonstructural protein 4B (NS4B) PDZ-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 translocation mediates the accumulation of Snail via activation of the p38 MAPK pathway.
The two PDZ domains within the PDZ34 tandem of Scribble, a cell polarity regulator, tightly pack in a 'front-to-back' mode to form a compact supramodule.
High levels of mislocalized SCRIB functions as a neomorph to promote mammary tumorigenesis.
miR-296-5p/SCRIB axis plays a role in breast carcinogenesis
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