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Validated All-in-One™ qPCR Primer for KLF4(NM_001314052.2) Search again
Product ID:
HQP165636
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
EZF, GKLF
Gene Description:
KLF transcription factor 4
Target Gene Accession:
NM_001314052.2(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.
Gene References into function
- This is the first paper that describes the identification and characterization of KLF4 (also called GKLF) and that KLF4 is inhibitor of cell growth.
- This paper describes that the nuclear localization signals within KLF4 define a closely related subfamily of Kruppel-like factors including KLF1, KLF2 and KLF4.
- This study examines the expression of KLF4 during embryonic and postnatal development and in intestinal tumorigenesis.
- This paper reports a consensus DNA binding sequence for KLF4 using an unbiased screen.
- This study reports the first identified target gene for KLF4 was CYP1A1, and the mechanism by which KLF4 regulates CYP1A1 expression.
- This study characterized the gene and promoter structures of the mouse KLF4 gene.
- This paper examines the structure-function relationship of KLF4 in activating target gene expression and in suppressing growth.
- This paper describes that KLF4 is transcriptionally activated by the p53 tumor suppressor after DNA damage and results in the transcriptional activation of the p21 cell cycle inhibitor gene.
- This paper reports that KLF4 is regulated by the APC tumor suppressor in colorectal cancer cells through CDX2.
- This paper describes the opposite effect of KLF4 and KLF5 on transcription of the KLF4 gene.
- induction of GKLF mRNA and protein expression by interferon-gamma treatment was associated with reduction of ornithine decarboxylase (ODC) gene expression and enzyme activity in colon cancer HT-29 cells
- KLF4 is an essential mediator of p53 in controlling G(1)/S progression of the cell cycle following DNA damage
- down-regulation of gut-enriched Kruppel-like factor in esophageal squamous cancer
- role in cell cycle regulation and epithelial differentiation
- Over-expression of KLF4 in human colon cancer cells reduces tumorigenecity.
- Regulation of A33 antigen expression by GKLF.
- inactivation of KLF4 is one of the frequent steps towards bladder carcinogenesis
- intestinal alkaline transactivation by Kruppel-like factor-4 is likely mediated through a critical region located within the proximal IAP promoter region
- KLF4 is necessary for preventing the entry into mitosis following DNA damage
- role of KLF4 in maintaining the integrity of the G2/M checkpoint following DNA damage
- KLF4 can act to repress histidine decarboxylase gene expression by Sp1-dependent and -independent mechanisms
- KLF4 is a tumor suppressor in colorectal cancer.
- KLF4 is a novel regulator of u-PAR expression that drives the synthesis of u-PAR in the luminal surface epithelial cells of the colon
- transactivation of Kruppel-like factor 4(KLF4) by butyrate appears to be mediated through interaction with a Sp1 transcription factor-binding domain on the promoter
- KLF4 has a role in the aggressive phenotype of early-stage infiltrating ductal carcinoma
- a longer isoform of gut-enriched Kruppel-like factor 4 (GKLF) we term GKLFa interacts with the CD11d promoter
- KLF4 can function in the nucleus to induce squamous epithelial dysplasia.
- A review article that summarizes the mechanisms by which KLF4 and KLF5 regulate cell proliferation.
- Promoter hypermethylation and hemizygous deletion contributed to the down-regulation of KLF4 expression and the induction of apoptosis contributed to the antitumor activity of KLF4; alteration of KLF4 expression plays a role in gastric cancer development
- KLF4 is both necessary and sufficient in preventing centrosome amplification following gamma-radiation-induced DNA damage.
- the cross talk of KLF4 and beta-catenin plays a critical role in homeostasis of the normal intestine as well as in tumorigenesis of colorectal cancers.
- cGMP-dependent protein kinase expression is regulated by Rho and Kruppel-like transcription factor-4
- KLF4 may be an important determinant of cell fate following gamma-radiation-induced DNA damage.
- KLF4 exerts a global inhibitory effect on macromolecular biosynthesis that is beyond its established role as a cell cycle inhibitor.
- KLF-4 and AP-2 is regulating the activity of the hSMVT promoter in the intestine and provide direct in vivo confirmation of hSMVT promoter activity.
- Kruppel-like factor 4 as a novel regulator of endothelial activation in response to pro-inflammatory stimuli.
- A review article that summarizes the biological and pathobiological functions in the intestinal epithelium.
- Genetic and epigenetic alterations of the KLF4 gene might play a minor role in gastric carcinogenesis.
- This study reports that haploinsufficiency of Klf4 gene in transgenic mice with targeted deletion of one of the Klf4 alleles promotes intestinal tumorigenesis when crossbred with the ApcMin mice.
- analysis of SNPs, located in the KLF2, KLF4 and KLF5 gene did not show an association with Type 2 diabetes in this French population
- KLF4 is a critical regulator in the transcriptional network controlling monocyte differentiation.
- KLF4 might function as an activator or repressor of transcription depending on whether it interacts with co-activators such as p300 and CREB-binding protein or co-repressors such as HDAC3.
- Data show that human testis strongly expresses KLF4 and they were localized to nuclei of round spermatids during normal spermatogenesis stages II-IV.
- Transient transfection of Kruppel-like factor 4 suppressed LDLR, steroidogenic acute regulatory protein, and CYP11A
- Using ectopic expression of Oct4, Sox2, Klf4 and Myc, we have derived iPS cells from fetal, neonatal and adult human primary cells
- Loss of KLF4 protein expression might contribute to assessing prognosis in colorectal cancer with lymph node metastasis
- KLF4 expression is associated with human skin SCC progression and metastases
- The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation
- Reduced levels of KLF4 tumor suppressor activity in colon tumors may be driven by elevated beta-catenin/Tcf signaling.
- Notch signaling suppresses KLF4 expression in intestinal tumors and colorectal cancer cells