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Validated All-in-One™ qPCR Primer for DCC(NM_005215.3) Search again
Product ID:
HQP094471
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
CRC18, CRCR1, HGPPS2, IGDCC1, MRMV1, NTN1R1
Gene Description:
DCC netrin 1 receptor
Target Gene Accession:
NM_005215.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- Altered expression of DCC protein is detectable in gastric carcinomas, an event that may have a role in the development of the disease.
- The netrin-1 receptor DCC promotes filopodia formation and cell spreading by activating Cdc42 and Rac1.
- Loss of dcc gene expression is associated with acute myelogenous leukemia
- loss of DCC expression occurs in some colon adenomas, but is insufficient to drive the adenoma to carcinoma progression.
- data suggest that the codon 201 polymorphism of the DCC gene was a target of LOH, and predicted prognosis in colorectal cancer patients
- DCC binds to netrin, which regulates its interactions with heparin
- Prognostic significance of the DCC gene protein expression in high-risk resected gastric carcinoma
- Deletions in this gene are found in colorectal and gastric cancers
- Multiple aberrations involving the DCC locus may play a role in the progression of nephroblastomas, and hence confer a poorer prognosis.
- DCC/netrin-1 signaling may commit cells to the transition of endometrial gland architecture or function from a proliferating to a secretory phase.
- Binding of netrin-1 to its receptors inhibits tumour suppressor p53-dependent apoptosis (review)
- DCC binds netrin through the fourth fibronectin type III domain.
- DCC expression appears not to be predictive in poor survival outcome in patients with stage II or III colorectal cancer.
- DCC in both commissural neurons and immortalized cells, is partially associated with cholesterol- and sphingolipid-enriched membrane domains named lipid rafts.
- The present study points to a potential influence of folates in regulating DCC expression at multiple levels involving post-transcriptional pathways.
- the localization of DCC to lipid rafts is a prerequisite for its proapoptotic activity, both in immortalized cells and in primary neurons
- Finds a linkage between the chromosome 18 near marker D18S851 at the third time point and the levels of HDL cholesterol in human males.
- Results suggest that DCC could regulate cell adhesion and migration through its association with ERM-M (ezrin/radixin/moesin and merlin) proteins.
- Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0% compared with 33% of those with high DCC expression (P = 0.0067).
- DCC is a putative conditional tumor-suppressor gene that is epigenetically inactivated by promoter hypermethylation in a majority of head-and-neck squamous cell carcinomas.
- Overexpression of the DDC gene in the LNCaP prostate cancer cell line leads to differential expression of a total of 35 genes.
- study provides evidence that most colorectal cancers have alterations in both UNC5C and DCC netrin receptors; while UNC5C expression is regulated primarily via epigenetic regulation, DCC defects are mediated through allelic deletions
- DCC methylation is a frequent and cancer-specific event in primary ESCCs (esophageal squamous cell carcinoma), suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target.
- DCC can be found in raft and non-raft portions of the plasma membrane.
- the transcriptionally active TAp73alpha tumor suppressor is implicated in the apoptosis induced by netrin-1 in a p53-independent and DCC/ubiquitin-proteasome dependent manner.
