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Validated All-in-One™ qPCR Primer for DKK1(NM_012242.3) Search again
Product ID:
HQP096323
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DKK-1, SK
Gene Description:
dickkopf WNT signaling pathway inhibitor 1
Target Gene Accession:
NM_012242.3(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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a protein that is a member of the dickkopf family. It is a secreted protein with two cysteine rich regions and is involved in embryonic development through its inhibition of the WNT signaling pathway. Elevated levels of DKK1 in bone marrow plasma and peripheral blood is associated with the presence of osteolytic bone lesions in patients with multiple myeloma. [provided by RefSeq].
Gene References into function
- overexpression sensitizes brain tumor cells to apoptosis after DNA alkylation damage; may link WNT and p53 pathways
- Analysis of individual Dkk domains & chimeric Dkks shows that the carboxy-terminal domains of both Dkk1 & 2 associate with LRP6 & are necessary & sufficient for Wnt8 inhibition. The NH2-terminal of Dkk1 plays an inhibitory role in Dkk-LRP interactions.
- dickkopf-1 has a critical role in reentry into the cell cycle of human adult stem cells from bone marrow
- Recombinant DKK1 inhibits the differentiation of osteoblastic precursor cells
- Data show that DKK1 decreass melanocyte function, probably through beta-catenin-mediated regulation of microphthalmia-associated transcription factor activity, which in turn modulates the growth and differentiation of melanocytes.
- Induction of DKK1 contributes to the pathological cascade triggered by beta-amyloid and is critically involved in the process of tau phosphorylation.
- Together, our data suggest that Dkk-1 may be able to antagonize Wnt signaling and exert its tumor suppressive effects through beta-catenin-independent non-canonical pathways (i.e., the Wnt/JNK pathway).
- Data show that FGF20 and DKK1 appear to be direct targets for beta-catenin/TCF transcriptional regulation via LEF/TCF-binding sites, and are expressed early in Xenopus embryogenesis under the control of the Wnt signaling pathway.
- DKK-1 expression decreases in human colon tumors, suggesting that DKK-1 acts as a tumor suppressor gene in this neoplasia; the Wnt/beta-catenin pathway is downregulated by the induction of DKK-1 expression, a mechanism that is lost in colon cancer
- We found that Dkk1-Fz5, but not Dkk3-Fz5, potently synergized with LRP6 to activate signaling in a dishevelled-dependent manner.
- These data suggest that HBM mutant proteins can transit to the cell surface in sufficient quantity to transduce Wnt signal and that the likely mechanism for the HBM mutations' physiologic effects is via reduced affinity to and inhibition by DKK1.
- Marrow stromal cell-conditioned medium promotes the proliferation of Dickkopf-1-secreting multiple myeloma cells.
- DKK-1 promoter was selectively hypermethylated in advanced colorectal neoplasms
- loss of DKK expression plays a role in development or progression of malignant melanoma
- reduction of DKK-1 levels after autologous stem cell transplantation may correlate with the normalization of osteoblast function
- The involvement of Dkk1 in human but not murine adipogenesis indicates that inter-species differences exist in the molecular control of this process.
- Dkk-1 and Dkk-4 may potentially be involved in the development of different injuries in response to pathological gastroesophageal acid reflux.Dickkopf homologs in squamous mucosa of esophagitis patients are overexpressed in Barrett's esophagus.
- The demonstration that DKK1 inhibits Wnt signaling in neurons and causes neuronal death supports the hypothesis that inhibition of the canonical Wnt pathway contributes to the pathophysiology of neurodegenerative disorders.
- Together, our data indicate the possible correlation between Dkk-1 and human placental choriocarcinoma and suggest potential applications of Dkk-1 in treatment of human placental choriocarcinomas.
- DKK1 is a key player in multiple myeloma bone disease
- These results further clarify the mechanism by which DKK1 suppresses melanocyte density and differentiation, and help explain why DKK1-rich palmoplantar epidermis is paler than non-palmoplantar epidermis via mesenchymal-epithelial interactions.
- Dickkopf-1 is a master regulator of joint remodeling.
- DKK1 as a potential prognostic and diagnostic marker for cohorts of breast cancer patients with poor prognosis. Dickkopf-1 may also become a relevant candidate target for immunotherapy of different cancers.
- Oxidative stress response regulates DKK1 expression through the JNK signaling cascade in multiple myeloma plasma cells.
- Inappropriate histone modifications might deregulate DKK1 expression in medulloblastoma tumorigenesis and block its tumor-suppressive activity.
- Calcitriol activates the transcription of the DKK-1 gene, probably in an indirect way that is associated to the promotion of a differentiated phenotype in colon cancer cells.
- DKK1 and SFRP1 inhibit the transformed phenotype of breast cancer cell lines, and DKK1 inhibits tumor formation.
- MYCN might stimulate cell proliferation by inhibiting the expression of DKK1. DKK1 might exert part of its growth suppressive effect by induction of SYNPO2 expression.
- data strongly suggests that dihydrotestosterone-inducible DKK-1 is involved in dihydrotestosterone-driven balding
- concludes that bone-derived prostate cell line that produces osteoblastic lesions induces new bone formation through Wnt canonical signaling, that LRP5 mediates this effect, and that DKK1 is involved in the balance between bone formation and resorption
- In 60 multiple myeloma patients checked, it was found that among the Wnt inhibitors, Dickkopf-1 and secreted frizzled-related protein-3 were produced by multiple myeloma cells.
- Increased Dickkopf-1 expression is associated with breast cancer bone metastases
- findings further elucidate why human skin is thicker and paler on the palms and soles than on the trunk through topographical and site-specific differences in the secretion of DKK1 by dermal fibroblasts that affects the overlying epidermis.
- Data demonstrate that systemic levels of Dkk-1 are elevated in osteosarcoma (OS) and may serve as a prognostic or diagnostic marker for evaluation of OS.
- DKK-1 mediated tumor suppressor effect is independent of beta-catenin dependent transcription and a CamKII pathway contributes to DKK-1 signaling
- Significant association with late-onset Alzheimer's disease for 4 SNPs: rs1881747 near DKK1, rs2279420 in ANK3, rs2306402 in CTNNA3, and rs5030882 in CXXC6 in 1,160 cases and 1,389 controls.
- Dkk1 inhibits this process and may be a key factor regulating pre-osteoblast differentiation and myeloma bone disease
- MesP1 drives vertebrate cardiovascular differentiation through Dkk-1-mediated blockade of Wnt-signalling
- DKK1 may play a key role in the development of osteolytic bone lesions in multiple myeloma by directly interrupting Wnt3a-regulated differentiation of osteoblasts
- Using a large series of myeloma patients, we could show for the first time a correlation between DKK-1 serum concentration and the amount of lytic bone disease, indicating that DKK-1 is an important factor for the extent of bone disease
- ASH1 inactivates DKK1 and DKK3, negative regulators of Wnt/beta-catenin signaling, E-cadherin, and integrin beta1 through ASH1-mediated deacetylation and repressive trimethylation of lysine 27 of histone H3 in the promoter regions of DKK1 and E-cadherin.
- Down-regulation of the Dkks associated to promoter hypermethylation appears to be frequently involved in gastrointestinal tumorigenesis.
- Kremen may not be essential for Dkk1-mediated Wnt antagonism and Kremen may only play a role when cells express a high level of LRP5/6
- DKK1 inhibition of LRP6 is independent of LRP6 internalization and degradation
- DKK1 and sclerostin are independent, and not synergistic, regulators of LRP5 signaling and that the function of each is impaired by HBM-LRP5 mutations
- Breast cancer-produced Dkk1 may be an important mechanistic link between primary breast tumors and secondary osteolytic bone metastases.
- Elevated DKK-1 expression is an early event in prostate cancer (PCa) and that as PCa progresses DKK-1 expression declines, particularly in advanced bone metastases.
- Dkk-1 secreted by mesenchymal stem cells inhibits growth of breast cancer cells via depression of Wnt signalling.
- DKK1 regulates distinct internalization pathways of LRP6 to tune the activation of beta catenin signaling.
- FHL2-beta-catenin interaction potentiates beta-catenin nuclear translocation and TCF/LEF transcription, resulting in increased Runx2 and alkaline phosphatase expression, which was inhibited by the Wnt inhibitor DKK1.
- Increased Dickkopf-1 blood levels were associated with a higher risk of progression of bone erosion, independently of age, sex, baseline radiological damage, C-reactive protein, and disease activity in Rheumatoid Arthritis patients.
- Serum DKK-1 levels are increased in prostate cancer patients.
- Dkk1 and sFRP4 perform an important function in adipogenesis in human adipose tissue-derived mesenchymal stem cells.
- myeloma cells are the main source of circulating DKK-1 protein and provide a framework for clinical trials on anti-DKK-1 treatment in multiple myeloma
- Dkk1 may play an important role in downregulating self-renewal and proliferation pathway of stem cells at the late stage of differentiation, and its failure may lead to carcinogenesis.