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Based on the variable expressivity and incomplete penetrance present in heterozygous carriers of a DCC variant, classification and clinical interpretation of missense variants is challenging in the absence of evidence of pathogenicity originated from functional studies
Study results indicate that DCC controls corticospinal tract midline crossing in both humans and mice, and that this process is non cell-autonomous in mice.
rs2229080 and rs7504990 polymorphisms in DCC might be related with breast cancer susceptibility in Chinese women.
Somatic DCC mutations are associated with metastatic NUT midline carcinoma.
Authors demonstrate that tripartite motif protein 9 (TRIM9)-dependent ubiquitination of DCC blocks the interaction with and phosphorylation of FAK.
Environmental and endogenous proteases may contribute to cancer development by depleting DCC and neogenin.
Identified DCC mutations in four families.
DCC polymorphism maybe responsible for successful treatment of patients with hydrochlorothiazide . diagnosed with hypertension.
Deleted in colorectal cancer (DCC) confers susceptibility to depression-like behaviors in humans and mice and Is regulated by miR-218. By regulating DCC, miR-218 may be a switch of susceptibility versus resilience to stress-related disorders.
DCC/18q and ERBB2/17q gene copy number variations are associated with disease-free survival in microsatellite stable colon cancer
Allelic and genotypic frequencies of the DCC polymorphism rs2229080 were nominally associated with schizophrenia.
Results of APC and DCC LOH, KRAS and microsatellite instability indicate our colorectal cancer cases were typical of sporadic cancers following the 'chromosomal instability' pathway.
The study identified DCC as a differentially expressed gene and clustered meningiomas into DCC low expression (3 grade I and 3 grade II tumors), DCC medium expression (2 grade I and 1 grade II tumors), and DCC high expression (5 grade I tumors) groups.
Data suggest that, in response to netrin-1/netrin receptor (DCC) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src homology 2 domains exhibit scaffolding properties sufficient to support axon outgrowth.
By analyzing multiple myeloma-derived cell lines and patient-derived primary CD138-positive plasma cells ... authors show for the first time that transcriptional dysregulation of DCC is involved in the progression of plasma cell malignancy.
the transfected DCC gene can suppress cell proliferation and lead to downregulation of CEA expression in SW1116 cells.
Signaling mechanism of the netrin-1 receptor DCC in axon guidance
NTN1-DCC pathway contains targets of FDA-approved drugs and may offer promise for guiding applied clinical research on preventive and therapeutic interventions for AMD
DCC mutation correlated with fractionated mirroring in individuals with Congenital mirror movements
Data show that silencing ezrin-radixin-moesin (ERM) protein expression ablates deleted in colorectal carcinoma protein (DCC)-protein kinase A (PKA) interaction and specifically blocks netrin-induced PKA activity and phosphorylation.
Schwann cell and dcc-mediated guidance are critical early during regeneration to direct growth cones across the transection gap and onto their original axonal trajectory.
in dcc mutants, turns on the inappropriate side of the body are caused by aberrant ipsilateral axonal projections
Dcc-Netrin1 and roundabout2 (Robo2)-Slit coordinate axonal projection choices of neurons in the developing forebrain.
Dcc regulates polarized axon initiation and asymmetric outgrowth of forebrain neurons
dcc may play roles not only in axon guidance, but in morphogenesis and functioning of these organs as well
First evidence that Netrin/DCC axon guidance molecules act in dendrites in a vertebrate system.
this work establishes a novel role for MARCKS in axon dynamics and highlights the necessity of MARCKS as an organizer of DCC signaling at the membrane.
Local spinal cord defects following loss of Dcc cause a hopping gait in mice and may contribute to mirror movements in humans.
We show, for the first time, that dopamine axons continue to grow from the striatum to the PFC during adolescence. Importantly, we discover that DCC, a guidance cue receptor, controls the extent of this protracted growth by determining where and when dopamine axons recognize their final target.
role in normal innervation of the peripheral vestibular system
Together, these results demonstrate that the production of DCC splice variants controlled by NOVA has a crucial function during many stages of commissural neuron development.
Results show that deleted in colorectal cancer receptors contribute to the dynamic refinement of dopamine D1 and D2 receptor expression in striatal regions across adolescence. The age-dependent expression of dopamine receptor in C57BL6 mice shows marked differences from previous characterizations in rats.
Results suggest that Netrin1/DCC signaling induce neuronal migration in the dorsal spinal cord.
Results suggest that Dcc plays an important role in the developmental formation of peripheral and central auditory circuits, and its mutation may contribute to sensorineural hearing loss.
dcc haploinsufficient mice acquire intracranial self-stimulation behavior and that the parameters of the stimulation are comparable to those observed in wild-type littermates; reduced expression of dcc may dampen the abuse potential of cocaine
Identified the Dcc gene as a novel downstream target of spontaneous calcium activity involved in axon growth.
suggest that DCC signaling functions through NCK1 and NCK2 and that both proteins are necessary for the establishment of normal spinal circuits necessary for gait
Results suggest that down syndrome cell adhesion molecule collaborates with deleted in colorectal cancer to regulate microtubule dynamics via direct binding to dynamic TUBB3 in Netrin-1-induced axon branching.
Overall, these findings suggest that commissural axons use distinct mechanisms to navigate in different CNS regions.
Data indicate the roles of Slit1/Robo1 and Netrin1/DCC signals in positioning motor neuron cell bodies.
These data demonstrate robust cardioprotective effect of netrin-1 in vivo, as shown by reduced infarct size and improved cardiac function mediated by netrin-1 receptor DCC.
Unc5C and DCC act downstream of Ctip2 and Satb2 and contribute to corpus callosum formation.
DCC appears to have a somewhat limited role in methamphetamine consumption and seeking following abstinence
The DCC expression by oligodendrocytes is required for the maintenance and stability of myelin in vivo, which is essential for proper signal conduction in the cenreal nervous system.
ESCRT-II-mediated endocytic pathway regulates both DCC and local protein synthesis.
This gene encodes a netrin 1 receptor. The transmembrane protein is a member of the immunoglobulin superfamily of cell adhesion molecules, and mediates axon guidance of neuronal growth cones towards sources of netrin 1 ligand. The cytoplasmic tail interacts with the tyrosine kinases Src and focal adhesion kinase (FAK, also known as PTK2) to mediate axon attraction. The protein partially localizes to lipid rafts, and induces apoptosis in the absence of ligand. The protein functions as a tumor suppressor, and is frequently mutated or downregulated in colorectal cancer and esophageal carcinoma.
colorectal cancer suppressor
, colorectal tumor suppressor
, deleted in colorectal cancer protein
, immunoglobulin superfamily DCC subclass member 1
, immunoglobulin superfamily, DCC subclass, member 1
, netrin receptor DCC
, tumor suppressor protein DCC
, deleted in colorectal carcinoma
, deleted in colorectal cancer
, deleted in colorectal cancer tumor suppressor
, netrin receptor DCC-like