Krueppel-like factor 2 Antibodies

Krueppel-like factor 2 (KLF2)

Transcription factor that binds to the CACCC box in the promoter of target genes such as HBB/beta globin or NOV and activates their transcription. .

Gene Information

Human
Gene Name:	KLF2
Uniprot:	Q9Y5W3
Entrez:	10365

Family

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

Alternative Names

KLF2; Krueppel-like factor 2; Kruppel-like factor 2 (lung); Kruppel-like factor LKLF; LKLF; LKLFLung krueppel-like factor; lung Kruppel-like zinc finger transcription factor

Molecular Weight

Mass (kDA):
37.42 kDA

Genomic Context

Human
Location:	19p13.11
Sequence:	19; NC_000019.10 (16324826..16328685)

Subcellular Localizations

Nucleus.

Diseases

• Atherosclerosis
• Inflammation
• Tissue Adhesions
• Malignant Neoplasms
• Neoplasms
• Tumor Angiogenesis
• Diabetes Mellitus
• Pathologic Neovascularization
• Thrombosis
• Cardiovascular Diseases
• Hypertensive Disease
• Vascular Diseases

• Vasculitis
• Leukemia
• Anemia
• Inflammatory Response
• Obesity
• Carcinoma

Interacting Proteins

• KAT2B
• SMURF1

Pathways

• Angiogenesis
• Cell Cycle
• Cell Adhesion
• Cell Activation
• Localization
• Cell Differentiation
• Pathogenesis
• Cell Proliferation
• Cell Migration
• Lung Development
• Inflammatory Response
• Secretion
• Cell Growth

• Vasculogenesis
• Cytokine Production
• T Cell Activation
• Coagulation
• Cell Development
• Cell Death
• Endothelial Cell Activation

PTMs

• Phosphorylation
• Methylation
• Acetylation
• Deacetylation
• Geranylgeranylation

• Ubiquitination
• Demethylation
• Nitrosylation
• Nitration
• Farnesylation

• Oxidation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/KLF2

Best Uses of the KLF4 Marker

The KLF4 genes regulate gene expression by modulating the histone acetylation. It is important to understand gene transcription and the KLF4 function. This article will explore the regulation, function, and applications of this gene. Let's begin. What does the KLF4 marker do? Here are some facts

Klf4 regulates gene transcription by modulating histone acetylation

The role of KLF4 is not yet fully understood. It is an essential regulator of DNA methylation, and plays an important role for stem cell maintenance. It is necessary for the production pluripotent stem cell from normal fibroblast cells. However, its role as a gene activator remains unclear. KLF4 interacts CREB binding protein, which has a catalytic HPAT domain. KLF4 interacts with CREB-binding proteins (CBP), which binds DNA sequence-specific transcription factor. CBP and KLF4 encourage localized histone acetylation through chromatin modification.

KLF4 is part of the Kruppel like factors family of transcription factors that includes zinc finger transcription. It is involved in cell proliferation, differentiation, apoptosis, as well as tumor suppression in colorectal carcinoma. It also regulates the reprogramming differentiation cells to pluripotent cells. It interacts with the p300 in vitro as well as in vivo.

VSMCs are developed by suppressing KLF5 expression. However, this suppression is reactivated upon stimulation of KLF8 by myocardin or vascular injury. This suggests that KLF8-dependent regulation KLF5 expression might be critical in the development the contractile phenotype VSMC.

The lncRNA HOTAIR was also implicated in the switching from acetylation and methylation of histone H3 Lysine 27. Activating KLF5 can increase tumorigenicity and resistance. It also inhibits the progression and spread of gastric cancer by blocking HDAC3.

Numerous other studies have shown Klf4 promotes EMT by modulating histone Acetylation. This protein is responsible for EMT and also contributes in other ways, such as N cadherin and E-cadherin. The mechanisms that drive this process remain elusive. It is important to monitor Klf4 expression to better understand its role in cancer development.

Furthermore, the identification and treatment of specific functions of Klf4 could be a novel approach to cancer treatment. Its regulation may provide a unique opportunity to target EMT tumors. Its role in cancer will be further explored. It is vital to recognize that Klf4 regulates transcription through modulating histone-acetylation.

Function

The Kruppel-like factor 2 (KLF2) gene is a zinc finger transcription factor and is an important regulator of endothelial quiescence and anti-inflammatory and antithrombotic responses. It also regulates blood flow and inhibits monocyte activation during inflammatory signals. Recent research has demonstrated that KLF2 is involved in the transcriptional regulation and differentiation of monocytes.

KLF2 was initially discovered in an adult mouse lung. The marker is present in embryogenesis and lymphoid cells. KLF2 is expressed in adult tissues as well as in the endothelium at the beginning of embryogenesis. The National Center for Biotechnology Information published research that showed KLF2 regulates certain protein release in various tissues including the lung, kidney, and heart.

Loss of KLF2 increases the number of macrophages in peripheral metabolic organs and contributes to the development of obesity and metabolic diseases. KLF2 loss results in an increase in macrophages and markers. It is therefore important to determine the genetic basis for metabolic diseases and to understand KLF2's contribution to it. KLF2 could be used to treat metabolic diseases if it is confirmed that it is essential.

To test if the KLF2 gene plays an important role in the downstream VEGFR2 signaling pathway, the researchers performed immunohistochemistry. They used antibodies against total VEGFR2, VEGFR2/1059, and Y951. The study was performed in patients after written informed consent. Immunohistochemistry were performed on the PCa tissue, as well as nearby normal tissues. The tissues were fixed in formalin and embedded in paraffin for 4 mm thick sections.

The EPC-diffusion process involves the KLF2 gene. This gene is believed to bind with the promoter to the vWF. In fact, Hough et al. Hough et.al. found that KLF2 binding increased the fluorescence in the luciferase asay. They were unable however to determine if this interaction between KLF2and vWF affected significantly the level of vWF.

Applications

The KLF2 human transcription factor is found in the KLF2 genes. Its DNA sequence is between 118 and 150 amino acids long. Recombinant production can be achieved by using polynucleotides with the KLF2 sequence. The polynucleotides then link to a promoter and are transformed into host cell. When they make up at least 80% of the sample, polynucleotides can be considered "substantially purified".

The KLF2 gene promoter can be linked with a gene expressing ligand. These genes are well-known in biology and are often selected because they are easy to detect and quantify. Next, the expression vector can be transferred to host cell. The marker gene expression level is measured when the test compound is present. The test compound's effect on statin-like and statin-antagonistic cells is determined by the difference in the results from infected cells and control cells.

One study used KLF2 as a marker for inflammatory diseases. In vitro experiments revealed that bone marrow-derived neutrophils from C57BL/6WT mice were treated using AngII. This reduced Klf2 levels in neutrophils. AngII treatment also induced expression of proinflammatory genes like Il1b, Tnfa and Ccl2.

KLF2 expression is a major factor in AngII-induced neutrophil activation as well as cardiac hypertrophy. KLF2 regulates neutrophil activation by interfering with HIF1-mediated signaling. It is also implicated with the pathogenic mechanisms of neutrophil-mediated immunethrombotic dysregulation. Hence, KLF2-NETosis-thrombosis interaction may prove to be an ideal therapeutic target in cardiovascular diseases.

Several studies have shown that the KLF2 gene is upregulated by increased shear stress. KLF2 also is expressed in the human orta at high shear stresses. The corresponding chicken embryo expression pattern is similar. High shear can be found at the OFT or inner curvature. It is expressed in both human and mouse endothelial cells.