Krueppel-like factor 5 Antibodies

Krueppel-like factor 5 (KLF5)

Transcription factor that binds to GC box promoter elements. Activates the transcription of these genes.

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Gene Information

Human
Gene Name:	KLF5
Uniprot:	Q13887
Entrez:	688

Family

Belongs to:
krueppel C2H2-type zinc-finger protein family

Alternative Names

Basic transcription element-binding protein 2; BTEB2; BTE-binding protein 2; CKLFGC-box-binding protein 2; Colon krueppel-like factor; colon kruppel-like factor; GC box binding protein 2; IKLFbasic transcription element binding protein 2; Intestinal-enriched krueppel-like factor; intestinal-enriched kruppel-like factor; KLF5; Krueppel-like factor 5; Kruppel-like factor 5 (intestinal); Transcription factor BTEB2

Molecular Weight

Mass (kDA):
50.792 kDA

Genomic Context

Human
Location:	13q22.1
Sequence:	13; NC_000013.11 (73054976..73077542)

Tissue Specificity

Expressed only in testis and placenta.

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Cell Transformation, Neoplastic
• Hyperplasia
• Mammary Neoplasms
• Malignant Neoplasm Of Breast
• Tumor Angiogenesis
• Carcinoma
• Carcinogenesis
• Hypertrophy
• Prostatic Neoplasms
• Cardiovascular Diseases
• Malignant Neoplasm Of Prostate

• Malignant Tumor Of Colon
• Inflammation
• Vascular System Injuries
• Haploinsufficiency
• Fibrosis
• Colorectal Cancer
• Hypertensive Disease

Interacting Proteins

• UBC

Pathways

• Cell Proliferation
• Cell Growth
• Cell Cycle
• Angiogenesis
• Pathogenesis
• Cell Differentiation
• Localization
• Methylation
• Cell Adhesion
• Rna Interference
• Oncogenesis
• Transport
• Cell Activation

• Cell Migration
• Proteolysis
• Cell Cycle Arrest
• Epithelial Cell Proliferation
• Mitosis
• Ossification
• Histone Acetylation

PTMs

• Phosphorylation
• Ubiquitination
• Acetylation
• Methylation
• Sumoylation

• Oxidation
• Demethylation
• Reduction
• Cleavage
• Deacetylation

• Dephosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/KLF5

Boster Bio: Best Uses Of The KLF5 Marker

This article will focus on the various uses of KLF5 in molecular biology. This marker is useful in many applications, including basal cells proliferation and permeability barrier function. We'll also cover how to perform colorimetric assays with this marker, and the safety of KLF5 for various applications. Continue reading to learn more. - Boster Bio: Best Uses Of The KLF5 Marker

KLF5 is a permeability barrier function

KLF5 is a vital molecule in CE homeostasis. It promotes proliferation of basal cells and regulates p27/Kip1 mRNA levels. The effects of KLF5 in CE markers is still not fully understood. Further research is therefore needed. KLF5 is a safe and effective way to increase CE barrier function for the moment.

Klf5 mutations result in corneal layers being reduced which results in decreased cell proliferation. This decrease is consistent with decreased cell proliferation across multiple tissues. The anti-Ki67 antibody led to a significant drop in the number of proliferating cell in Klf5D/DCE eyes. This is due to the reduction in cell layers and the decrease of Ki67+ cells per unit height of the central cornea.

This effect was observed in both the Klf5D/DCE mouse eye and control cornea. Klf5D/DCE mice had a basement membrane disruption. Klf5D/DCECE CE saw a decrease of Dsg1a/Dsg1a expression. Furthermore, transcriptions of several other desmosomal components were decreased and immunofluorescence staining revealed that the expression of these proteins is reduced in Klf5D/DCE CE. These results suggest that these factors could be contributing to the altered barrier function.

Klf5's N-terminal regulatory domains are different from Klf4's. Klf5 is not regulated by OCT1 and Klf5 have different target sites. While the results of cotransfections of OCT1 and KLF5 were encouraging, this effect could be reversed by adding KLF4 to the mix. These proteins compete for the same binding spot.

Proliferation of basal cell

KLF5 gene expression promotes cell growth, and migration. We tested this gene by transfecting HPASMCs using lentiviral vectors expressing KLF5 or a control vector. We found that KLF5 was knocked down in both right ventricular hypertrophy (pulmonary hypertension) and pulmonary hypertension (right ventricular hypertrophy). The KLF5 gene interacts with the transcription factor HIF-1. Knockdown HIF-1 was not able to alter KLF5's expression, but it did increase the number and ratios of Bax-to-Bcl-2 and cleaved capase-3.

The Kruppel family includes transcription factors that regulate many functions, including self-renewal and survival, as well as proliferation and self-renewal. This gene is expressed in the mouse embryo and adopts a tissue-selective pattern in adulthood. Because it has a role in regulating smooth muscle cell differentiation and proliferation, it has been identified as a cancer-related gene.

KLF5 expression was compared between BCR-ABL–abl-loop+ precursors of T-cells in normal adult BM, and BCR–ABL–ABL–loop+ cells from patients with acute Lymphoblastic Leukemia (AML). KLF5 mRNA levels were lower in leukemic B-cell precursors than in normal blood cells.

KLF5 has been linked to accelerated G1/S cell cycle progression in a variety models. KLF5 overexpression in human aortic smooth muscular cells and PHPASMCs caused rapid cell development with high levels cyclin B1. KLF5 inhibition by siRNA resulted in both decreased gene expression and inhibition of cyclin B1 activation.

KLF5 is essential to cell proliferation and differentiation. It regulates lineage formation in preimplantation mouse embryos. KLF5 is involved in a variety of cancers, in addition to its role during embryonic development. To understand the role of KLF5 in cancer development, further research is needed into the molecular mechanism of KLF5 Transactivation.

Colorimetric assays

Recent advances in DNA technology have allowed for the development and use of colorimetric methods to study human cell proliferation. These assays can be used to identify cell proliferation and can be combined with other cellular markers. This new technology opens up new possibilities for medical treatment monitoring as well as research. These assays can provide valuable information about the composition and activity of DNA in cells.

Moreover, KLF5 knockdown inhibits proliferation of HeLa cells, irrespective of TNF-a levels. TNFa-induced invasion and migration are suppressed in cells that have KLF5 knockdown. Hence, these findings support the role of KLF5 in autophagosome-mediated tumor suppression. This study also confirms the importance of KLF5 in regulating gene expression.

Recent research shows that knockdown KLF5 causes an increase in the accumulation of LC-3 II (and BECN1) proteins. Knockdown KLF5 increased BECN1 and decreased levels of p62, which are both autophagy substrates. KLF5 was overexpressed, which decreased LC3II accumulation. KLF5 was overexpressed, which increased BECN1 expression and p62.

To create a KLF5 knodown reporter plasmid, 948 bp were added to a base plasmid. We then used an X-tremeGENE HP DNA transfection reagent and a KLF5 knockdown subclone. Western blotting was used for this assay.

SimRNAs targeting a-Catulin, the cytoskeletal connecter protein, were used to transfect C4-2 with the KLF5 genes. The cells were then fixed in Karnovsky’s solution that contains 2% paraformaldehyde as well as 5% glutaraldehyde. The samples were then dried in ethanol.

Safety

Recent research has shown that KLF5 is associated with prostate cancer progression. Recent analysis found that the protein was correlated with both AR1-HSF1. Based on this association, the two proteins may be co-factors. The bioinformatics analysis predicted that AR and KLF5 may have a connection. However, separate analyses revealed that AR and KLF5 are independent cofactors.

KLF5 was one of the genes studied. It regulates metabolic and atrophy-related gene expressions. In addition to this, it may also be involved in the pathogenesis of human disuse muscle atrophy, a common consequence of prolonged physical inactivity. However, the exact role of KLF5 in this condition remains elusive. To fully understand this relationship, further studies are required. This study shows that KLF5 may be beneficial in the treatment of age-related muscle atrophy.

In addition to its role in cancer cell migration, KLF5 has also been associated with poor prognosis. Overexpression of KLF5 has been linked to aggressive clinical behavior. In a recent study, Yang et al. Yang et.al. identified KLF5 in bladder cancer as a poor prognosticator. Although this is a premature study, it does suggest that KLF5 could be a promising therapeutic target for patients with advanced cancer.

KLF5 regulation is not only important, but Foxo1 and dex induced transcription are also controlled by it. SNHG12 expression is also affected when KLF5 is silenced on CRC cell lines. This suggests that KLF5 is upstream of Foxo1 or STAT3.

Optimization

Boster Bio optimizes the KLF5 gene marker to allow for sensitive colorimetric cell proliferation tests. This marker can also be used to perform cytotoxicity tests. The KLF5 gene was found in the CE of adult mice. This gene contributes towards CE homeostasis by stimulating basal cell growth and suppressing phospho(Ser-10) p27/Kip1. It does not affect epithelial marker expression.