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Validated All-in-One™ qPCR Primer for KLF6(NM_001300.5) Search again
Product ID:
HQP092893
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCD1, CBA1, COPEB, CPBP, GBF, PAC1, ST12, ZF9
Gene Description:
KLF transcription factor 6
Target Gene Accession:
NM_001300.5(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 nuclear protein that has three zinc fingers at the end of its C-terminal domain, a serine/threonine-rich central region, and an acidic domain lying within the N-terminal region. The zinc fingers of this protein are responsible for the specific DNA binding with the guanine-rich core promoter elements. The central region might be involved in activation or posttranslational regulatory pathways, and the acidic N-terminal domain might play an important role in the process of transcriptional activation. It is capable of activating transcription approximately 4-fold either on homologous or heterologous promoters. The DNA binding and transcriptional activity of this protein, in conjunction with its expression pattern, suggests that this protein may participate in the regulation and/or maintenance of the basal expression of pregnancy-specific glycoprotein genes and possibly other TATA box-less genes. Two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq].
Gene References into function
- data suggest that KLF6 is a tumor suppressor gene involved in human prostate cancer
- KLF6 gene may be involved in carcinogenesis of sporadic nasopharyngeal carcinomas.
- Studies of binding of KLF6 to the human iNOS promoter reveal CACCC binding sites and transactivation of iNOS promoter in diverse pathophysiological conditions: NaCN-induced hypoxia, heat shock, serum starvation, and PMA/ionophore stimulation
- may act as a suppressor of prostatic cancer. (review)
- role in prostate cancers; significant genetic alterations of KLF6 occur in a minority of high-grade prostate cancers
- Mutations of the KLF6 gene play a role in the pathogenesis of astrocytic gliomas.
- Zf9 transcription factor represents an additional candidate susceptibility gene for investigating hereditary predisposition to Dupuytren disease.
- Deregulation of KLF6 by a combination of allelic imbalance and mutation may play a role in the development of colorectal cancer
- Our results provide the first evidence of functional tumor suppression by KFL6, and its loss may contribute to glial tumor progression.
- Altered mRNA expression is associated with prostate cancer recurrence.
- Diminished expression of KLF6 correlates with poor prognosis and high probability of therapy failure in prostate cancer patients.
- Transcriptional activation of the insulin-like growth factor I receptor gene by the Kruppel-like factor 6 (KLF6) tumor suppressor protein.
- KLF6 germ-like mutations are of marginal importance in prostate cancer predisposition in Finland.
- examination of role as potential tumor suppressor gene product
- KLF6 is deregulated by loss and/or mutation in hepatocellular carcinoma, and its inactivation may contribute to pathogenesis in a significant number of these tumors.
- genetic alterations of KLF6 gene might play an important role in the development or progression of sporadic gastric cancers
- Repression of Dlk1 requires HDAC3 deacetylase activity, which is recruited to the endogenous Dlk1 promoter where it interacts with KLF6. The interaction between HDAC3 and KLF6 is identified as a potential mechanism underlying adipogenesis.
- Absence of mutation in the putative tumor-suppressor gene KLF6 is demonstrated in colorectal neoplasms.
- KLF6 gene transcription is under control of a TATA-box independent initiation mechanism together with an evolutionary conserved array of positive cis-acting elements.
- Transcription factor KLF6 downregulates the alpha1-PI gene in corneal epithelial cells and may thereby be involved in keratoconus.
- These results provide the first characterization of the Acid Ceremidase promoter from any species and demonstrate that Kruppel-like factor 6 (KLF6) is one transcription factor involved in the regulation of AC gene expression.
- The negative association between KLF6 IVS1-27A and prostate cancer risk supports a population-specific effect of susceptibility alleles in prostate tumorigenesis.
- KLF6-mediated changes in E-cadherin levels are accompanied by downstream changes in both the subcellular localization of beta-catenin and c-myc expression levels.
- KLF6 and KLF6-SV1 are associated with key clinical features of ovarian cancer and suggest that their therapeutic targeting may alter ovarian cancer growth, progression, and dissemination.
- KLF6 gene may be one of the candidate tumor suppressor genes in colorectal cancers and that genetic alteration of the KLF6 gene might play a role in the development of colorectal carcinomas.
- The results suggest that genetic and epigenetic alteration of KLF6 may play a minor role in the development of hepatocellular carcinoma (HCC)
- KLF6 may be involved in pathogenesis of hepatocellular carcinoma
- Human transcription factors KLF2 and KLF6 are targets of the P. aeruginosa type III exoenzymes S and Y, with potential importance in host cell death.
- an SP2/KLF6 repression complex by SHP is required for farnesoid X receptor-induced endothelial cell migration
- Deregulation of KLF6 stability may alter its tumor suppressor function and/or the response of tumors to chemotherapeutics
- Association of KLF6 germline polymorphism with prostate cancer risk, but not benign prostatic hyperplasia risk in Finland.
- KLF6 coding sequences are altered in 10% brain tumors, 8% NSLC, and 4% of cancer cell lines.
- our results suggest a potential involvement of KLF6 polymorphisms in lung cancer risk
- Loss of heterozygosity of the KLF6 at chromosome 10p15 contributes to the invasion step from an intramucosal carcinoma to an invasive carcinoma specifically in sporadic colorectal carcinogenesis
- Data demonstrated that KLF6 is essential for hepatocellular carcinoma -derived cells to evade apoptosis.
- KLF6 allelic imbalance and decreased KLF6 and increased KLF6-SV1 expression are common findings in primary GBM tumors
- KLF6 loss of heterozygosity represents a clinically-relevant biomarker predicting patient survival and tumor recurrence
- KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not
- Expression of Sp1 and KLF6 is developmentally regulated, providing basis for further investigations on regulation of Sp1 and KLF6 gene during course of corneal development and in corneal diseases such as keratoconus.
- The CpG islands in TFPI-2 promoter was hypermethylated in highly invasive breast cancer cell line, and DNA methylation in the entire promoter region caused TFPI-2 repression by inducing inactive chromatin structure and decreasing KLF6 binding.
- Stimulation of KLF6 expression by IGF-I in a p53-dependent manner may constitute a novel mechanism of action of IGF-I, with implications in normal cell cycle progression and cancer biology.
- our results suggested that the IVS1 -27G/A polymorphism of KLF6 is not associated with an increased risk for gastric cancer in Korean population.
- Increased expression of KLF6-SV1 is associated with decreased survival in patients with lung adenocarcinoma.
- The Kruppel-like factor 6 (KLF6) gene is a zinc finger transcription factor that inhibits cellular growth in part by transcriptional activation of p21.
- functional polymorphism in the KLF6 gene is associated with advanced nonalcoholic fatty liver disease
- DAPK2 as a novel Sp1-dependent target gene for E2F1 and KLF6 in cell death response.
- KLF6 overexpression accelerates human prostate cancer progression and metastasis.
- expression of the KLF6 alternative splice forms was significantly increased in pancreatic tumour samples and cell lines. These cancers demonstrate marked cytoplasmic KLF6 expression but not a nuclear localisation signal.
- wtKLF6-transfected prostate cancer & renal carcinoma cell lines had less proliferation capacity & more apoptosis; more cells in G0/G1 & less in G2/M phases; and upregulated Cip1.
- KLF6 plays a permissive role in TGF-beta1-induced epithelial-mesenchymal transition in proximal tubule cells. Its upregulation in in vivo models of diabetic nephropathy suggests it as a potential therapeutic target.
- ATF3 is a key mediator of KLF6-induced apoptosis in prostate cancer cells
- KLF6 and TP53 mutations are not frequent events in prostate cancer