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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 (show TRIM9 Proteins))-dependent ubiquitination of DCC blocks the interaction with and phosphorylation of FAK (show PTK2 Proteins).
Environmental and endogenous proteases may contribute to cancer development by depleting DCC and neogenin (show NEO1 Proteins).
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 (show MLXIP Proteins)-218. By regulating DCC, miR (show MLXIP Proteins)-218 may be a switch of susceptibility versus resilience to stress-related disorders.
DCC/18q and ERBB2 (show ERBB2 Proteins)/17q gene copy number variations are associated with disease-free survival in microsatellite stable colon cancer
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.
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.
Together, these results demonstrate that the production of DCC splice variants controlled by NOVA (show HNRNPK Proteins) 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 (show DRD2 Proteins) 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 (show NCK1 Proteins) and NCK2 (show NCK2 Proteins) and that both proteins are necessary for the establishment of normal spinal circuits necessary for gait
ESCRT-II (show VPS28 Proteins)-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