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Validated All-in-One™ qPCR Primer for KLF5(NM_001730.4) Search again
Product ID:
HQP017898
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BTEB2, CKLF, IKLF
Gene Description:
KLF transcription factor 5
Target Gene Accession:
NM_001730.4(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 member of the Kruppel-like factor subfamily of zinc finger proteins. Since the protein localizes to the nucleus and binds the epidermal growth factor response element, it is thought to be a transcription factor. [provided by RefSeq].
Gene References into function
- Overexpression of KLF5 in transfected cells led to increased cell proliferation including foci formation and anchorage-independent growth in a manner consistent with a transformed phenotype.
- This study describes the opposite effect of KLF4 and KLF5 on transcription of the KLF4 gene.
- KLF5 suppresses tumor cell growth in breast cancer.
- KLF5 bound and efficiently transactivated the TCR Dbeta1 promoter
- Gene deletion and loss of expression and cell growth suppression indicate that KLF5 may be tumor suppressor gene at 13q21 in prostate cancer. Mutation and promoter methylation do not commonly inactivate KLF5 in prostate cancer.
- KLF4, but not KLF5, was frequently downregulated in bladder cancer cell lines and cancer tissues.
- KLF5 and p50 are important for induction of PDGF-A chain.
- BTEB2, a zinc finger transcription factor, may contribute to the establishment of the choroidal neovascularization observed in the pathogenesis of age-related macular degeneration and idiopathic choroidal neovascularization
- Positive and negative regulation of the cardiovascular transcription factor KLF5 by p300 and the oncogenic regulator SET through interaction and acetylation on the DNA-binding domain.
- intestinal tumor progression is associated with a change in the growth-related functions of KLF5
- KLF5 mediates the transforming effect of oncogenic H-Ras in NIH3T3 fibroblast cells and does so by transactivating the cyclin D1 promoter
- Results indicate that Kruppel-like factor 5 is a potential mediator for the inhibitory effect of all-trans retinoid acid on intestinal epithelial cell proliferation.
- This study describes that the inhibitory effect of all-trans retinoic acid (ATRA) on proliferation of intestinal epithelial cells is a result of ATRA-mediated expression of KLF5.
- HDAC1 negatively regulates the cardiovascular transcription factor KLF5 through direct interaction
- KLF5 protein is degraded at least in part through ubiquitination-proteasome pathway, which may have become hyperactive for KLF5 in cancer cells
- This is an review article that summarizes the function of KLF4 and KLF5 in regulating cell proliferation.
- In co-transfection assays in K562 cells, it was demonstrated that KLF2, 5 and 13 positively regulate, and KLF8 negatively regulates, the gamma-globin gene through the CACCC promoter element.
- KLF5 is a key component of the transcription factor network controlling adipocyte differentiation
- KLF5 is an essential transcription factor in cardiovascular remodeling (review)
- This study reports that KLF5 is activated by oncogenic HRAS and that activated KLF5 promotes mitosis by inducing transcription of the cyclin B1 and Cdc2 genes.
- KLF5 is a target of the E3 ubiquitin ligase WWP1 for proteolysis in epithelial cells
- KLF2 is a transcription factor important in the integration of multiple endothelial functions associated with regions of the arterial vasculature that are relatively resistant to atherogenesis.
- This study describes that KLF5 is an important downstream mediator for the pro-inflammatory activity of NF-kB in intestinal epithelial cells.
- analysis of a novel regulatory pathway for the expression of survivin under the control of KLF5 and p53
- Patients with higher KLF5 expression have shorter disease-free survival and overall survival than patients with lower KLF5 expression.
- This study examines the physical interaction between KLF5 and protein inhibitor of activated STAT 1 (PIAS1) which enhances KLF5's pro-proliferative activity.
- KLF5 protein degradation is blocked by an N-terminal FLAG tag or a small N-terminal deletion without reducing ubiquitination and degradation mediated by WWP1.
- KLF5 as a target of lysophosphatidic acid mediated signaling and suggest a role of KLF5 in promoting proliferation of intestinal epithelia in response to lysophosphatidic acid .
- A review article that describes the biological and pathobiological functions in the intestinal epithelium.
- Plays an important role in modulating apoptosis secondary to DNA damage through a p53-independent pathway
- analysis of SNPs, located in the KLF2, KLF4 and KLF5 gene did not show an association with Type 2 diabetes in this French population
- recruitment of ANP32B onto the promoter region requires KLF5 and results in promoter region-specific histone incorporation and inhibition of histone acetylation by ANP32B
- This study reports that KLF5 is an important downstream mediator for the transforming effect of activated KRAS in intestinal epithelial cells and colorectal cancer.
- These findings suggest that the KLF5 gene is a novel schizophrenia-susceptibility gene, and that the expression of the gene is involved in the pathophysiology of schizophrenia via glutamatergic neurotransmission.
- KLF5 causes cartilage matrix degradation through transcriptional induction of MMP9, providing the first evidence that transcriptional regulation of a proteinase contributes to endochondral ossification and skeletal development.
- Results suggest that the FASN gene is activated by the synergistic action of KLF5 and SREBP-1, which was induced by androgen in androgen-dependent prostate cancer cells.
- nuclear export signal in KLF5 directs a fused green fluorescence protein to the cytoplasm