ATF4 Antibodies

Cyclic AMP-dependent transcription factor ATF-4 (ATF4)

Transcriptional activator. Cooperates with FOXO1 in osteoblasts to regulate glucose homeostasis through suppression of beta-cell production and decline in insulin production (By similarity).

It binds to a Tax-responsive enhancer element in the long terminal repeat of HTLV-I. Regulates the induction of DDIT3/CHOP and asparagine synthetase (ASNS) in response to endoplasmic reticulum (ER) stress.

Gene Information

Human
Gene Name:	ATF4
Uniprot:	P18848
Entrez:	468

Family

Belongs to:
bZIP family

Alternative Names

activating transcription factor 4 (tax-responsive enhancer element B67); Activating transcription factor 4; ATF4; cAMP-dependent transcription factor ATF-4; cAMP-responsive element-binding protein 2; CREB-2DNA-binding protein TAXREB67; cyclic AMP-dependent transcription factor ATF-4; Cyclic AMP-responsive element-binding protein 2; TAXREB67; TAXREB67CREB2cAMP response element-binding protein 2; Tax-responsive enhancer element-binding protein 67; TXREB

Molecular Weight

Mass (kDA):
38.59 kDA

Genomic Context

Human
Location:	22q13.1
Sequence:	22; NC_000022.11 (39514494..39522686)

Subcellular Localizations

Cytoplasm. Cell membrane. Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Colocalizes with GABBR1 in hippocampal neuron dendritic membranes (By similarity). Colocalizes with NEK6 at the centrosome (PubMed:20873783).

Diseases

• Endoplasmic Reticulum Stress
• Malignant Neoplasms
• Neoplasms
• Physiological Stress
• Hypoxia
• Diabetes Mellitus
• Inflammation
• Carcinoma
• Leukemia
• Liver Carcinoma
• Nervousness
• Mammary Neoplasms

• Ischemia
• Anoxia
• Malignant Neoplasm Of Breast
• Obesity
• Growth Arrest
• Multiple Myeloma

Interacting Proteins

• ATF3
• BFSP2
• BTRC
• CCDC106
• CEBPA

• CEBPB
• CEBPD
• CEBPG
• CREBZF
• Dapk3

• DDIT3
• DISC1
• FOS
• GCC1
• GOLGA1

• GOLGA8DP
• GOLGA8F
• GPS2
• HAUS7
• JUN

• LDOC1
• NDC80
• NFE2L2
• POLR2C
• TRIB3

Pathways

• Translation
• Cell Death
• Osteoblast Differentiation
• Cell Cycle
• Pathogenesis
• Autophagy
• Secretion
• Cell Growth
• Transport
• Cell Proliferation
• Rna Interference
• Proteolysis
• Angiogenesis

• Response To Stress
• Induction Of Apoptosis
• Cell Differentiation
• Protein Folding
• Localization
• Drug Resistance
• Osteoblast Proliferation

PTMs

• Phosphorylation
• Cleavage
• Dephosphorylation
• Acetylation
• Ubiquitination
• Oxidation

• Deacetylation
• Methylation
• Biotinylation
• Hydroxylation
• Glycosylation
• Palmitoylation

Research Areas

• Lipid and Metabolism
• Phospho-Specific
• Unfolded Protein Response
• Unfolded Protein Response (UPR)

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATF4

Boster Bio Anti-ATF4 Marker - Biological Relevance, Validation, and Applications

In this article, we'll cover the Biological Relevance, Validation, and Applications of the Anti-ATF4 Marker. You've found the right place should you be looking for an item with high affinity and specificity. Boster's products can be tested on several platforms, and the company will give you product credits if you're one of the first to review them! We hope you found this article helpful and informative.

Anti-ATF4 Marker

The Anti-ATF4 Marker found in BoSTER Bio reagents interacts with human, mouse, and rat ATF4 proteins. This antibody is stable for a year at -20degC. Each Aliquot contains 5 mg BSA, 0.05mg Thimerosal, and 0.1 mg of NaN3. It recognizes the human ATF4 C-terminal mRNA region. It is also compatible with mouse and rat ATF4 sequences.

ATF4 expression was measured in human osteosarcoma tissue by fluorescence in situ hybridization (FISH) plus immunohistochemistry. Immunohistochemical analysis revealed that ATF4 protein and its mRNA levels were significantly lower in OS tissues than in normal tissues. These results suggest that ATF4 could play a role in the suppression of tumor growth. ATF4 is a key signaling molecule in apoptosis.

ATF4 is a transcriptional stress-inducing element. It is often upregulated in many cancers and is linked with resistance to chemotherapeutic drugs. Moreover, accumulating evidence supports the idea that ATF4 switches to a pro-apoptotic signalling. It forms heterodimers that are homologous to C/EBP protein and stimulates apoptosis in cancer cells that lack CHOP.

Leishmania is also caused by ATF4. Leishmania parasites activate eIF2a and ATF4 in macrophages. Knockout macrophages showed no increase in ATF4 expression or nuclear translocation. Infection-induced ATF4 expression in infected macrophages is also linked to the higher level of the HO-1. The immune response to Leishmania parasites is based on PERK/eIF2a/ signaling.

A small molecule known as monensin increases ATF4 activity within a variety cells. Monensin, a molecule that is similar to thapsigargin in the sense that it triggers phosphorylation in cells under nutrient stress it is also comparable to thapsigargin in that it induces phosphorylation of cells under stress. The results show the effectiveness of this therapy for anti-ATF4 antibodies. The anti-ATF4 Marker found in Boster Bio Reagents is a useful tool for biomarkers.

Applications

ATF4 is a transcription factor for leucine and zinc located on the chromosome 22,q13. This gene regulates metabolism in cells and amino acid biosynthesis as well as transporter activities. It also regulates the homeostasis of glucose. Its molecular mass is 50 kDa. The ATF4 marker has many applications such as gene therapy and cancer research. Recently it was found that ATF4 expression is very high in osteoblasts.

The transcription factor ATF4 plays a crucial role in regulating ER stress. Under stress oxidative, ATF4 stimulates a response known as the unfolded protein response (UPR). This signaling pathway activates a range of genes involved in the repair of DNA, cell proliferation and tumorigenesis. It is implicated in breast cancer and other cancers. This protein plays an important role in the metabolism of cells, such as osteogenesis, lipogenesis and adipogenesis. It plays a crucial part in regulating the ER stress response, which occurs when the cell is exposed to an event that causes stress.

There are numerous applications for the ATF4 gene involved in HSC differentiation. ATF4 upregulation in niche cells has been linked in the regulation of the expression of Angptl3 which is a crucial element in the expansion of functional HSCs. These findings have significant implications for the development of new therapeutic strategies to treat HSC expansion. This research will help to discover new ways to treat cancer. If you're looking for the best method to identify patients suffering from ATF4, you should start your research now.

ATF4 has also been linked to the development of neurological disorders like AIDS and ER stress. These conditions suggest that ATF4 is a key player in these disorders. However, more research is needed to determine its role in the development of these diseases. ATF4 is a candidate for use in a variety of areas of cancer research, for instance, in the detection of MS and in the prevention of the development of multiple tumors.

Validation

ATF4 is a member of the ATF/CREB transcription family that regulates gene expression. It is located on chromosome 22, and functions as a distinct CRE-dependent transcription repressor. Scientists can evaluate ATF4 activity with non-human primate samples by using the Boster Bio Antibody picoband. The antibody contains Trehalose and synthetic peptides, and can be stored at -20°C for one year , or four degrees C for a month.

Boster Bio validated the ATF4 marker by comparing the protein expression in hepatic cells with controls. They showed that elevated levels of ATF4 were associated with a decrease in the expression of the oxidative stress marker CSE. After one hour, however, ATF4 levels returned to levels that were previously found to be normal. This suggests that the oxidative stress induction of ATF4 requires the presence of cysteine to trigger.

The ATF4 protein was bound to two gene promoters: SLC7A11 and ATF3. The ATF4 expression was reduced due to the loss of YAP/TAZ, suggesting that ATF4 functions at a low level. Additionally, the binding of the marker to SLC7A11 promoter is regulated by the YAP/TAZ. Boster Bio's ATF4 marker therefore is highly specific and precise.

The depletion of ATF4 results in higher levels of ROS and the oxidation of lipids. Cell viability is affected by the reduction in intracellular GSH or cystine uptake. Ferroptostatin-1 also inhibits ATF4 loss. These results support the validity of the ATF4 marker in Boster Bio as a biomarker of ferroptosis.

Biological Relevance

The ATF4 marker has been implicated in a range of diseases, including retinal degeneration and neurodegenerative disorders. In addition, ATF4 expression has been associated with retinal degeneration in T17M rhodopsin mice. The mechanism through which ATF4 is able to promote angiogenesis remains unclear. Further research is needed to better understand the mechanism.

Independently of CHOP, ATF4 regulates 254 genes. These genes control cellular metabolism that includes amino acid biosynthesis and transporter activity. Although it's not necessary for cell function, its overregulation is associated with AD's pathological hallmarks. Additionally, it has been associated with an increase in phosphorylation tau and protein phosphatase-1 kinases, a hallmark of Alzheimer's disease.

In addition to its function in the life of cells In addition to its role in cell survival, the ATF4 marker is also involved in the degradative process of transcription factors that are RNA-dependent. ATF4 actually causes an imbalance in eIF2a–P which decreases transcription factors dependent on RNA. This interplay between oxidative stress and ER stress has been referred to as the "integrated stress response".

ATF4 could also have a regulatory effect on GRP78. It has been suggested that this protein plays a significant role in the regulation of ER stress and the oxidative stress. This gene could be targeted to offer new treatments for COVID-19 patients. It is therefore important to understand the role of the ATF4 in the development of this disease. ATF4 can help in preventing the development of the disease if it is managed properly.

Activation involves phosphorylation eIF2a which triggers it. It then controls the expression of target genes linked to pro-apoptotic CCAAT/enhancer-binding protein. The gene also has a conserved binding location (5'-TGACGTGA-3') upstream of the ER stress response element. This site is distinct from the C/EBP/ATF composite.

Gene Infographics

Genes that are associated with the ATF4 marker are referred to as transcription factors related to ATF4. The enzyme controls the expression of 254 genes independent of CHOP. The genes control the metabolism of cells, including amino acids biosynthesis and activation of transporters. Gene infographics for ATF4 will assist you in understanding the gene and the role it plays in the body. The gene is responsible for the regulation of a variety of functions in the body.

Research suggests that ATF4 might be a novel regulator of monocyte chemoattractant protein-1 (MCP-1), overproduced in the retina of mice during degeneration. This gene is vital for the maintenance of retinal function in mice and prevents photoreceptor cells from dying. It has also been associated with neurodegenerative diseases. It could be a potential drug target for diabetes.

Overexpression of ATF4 mRNA increased expression of several genes associated with apoptosis. The upregulation of ATF4 MRNA was associated with increased stress in the cell. The gene also regulates p53-mediated signaling and TNF/stress-related signaling. Different types of cancers are linked to ATF4's transcriptional regulation. Current research is in progress to discover the role played by ATF4 in the cell's development and function.

ATF4 is a key anabolic transcription factor in mTORC1 pathway. ATF4 is important in the synthesis of glutathione which is the body's strongest antioxidant. It also increases the production of glutathione. ATF4 has many other functions throughout the body, for instance, stimulating the growth of the mTORC1 pathway.