IRF5 Antibodies

Interferon regulatory factor 5 (IRF5)

Transcription factor involved in the induction of interferons IFNA and INFB and inflammatory cytokines upon virus infection. Activated by TLR7 or TLR8 signaling.

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Gene Information

Human
Gene Name:	IRF5
Uniprot:	Q13568
Entrez:	3663

Family

Belongs to:
IRF family

Alternative Names

IBD14; interferon regulatory factor 5; IRF5; IRF-5; SLEB10

Molecular Weight

Mass (kDA):
56.044 kDA

Genomic Context

Human
Location:	7q32.1
Sequence:	7; NC_000007.14 (128937032..128950042)

Subcellular Localizations

Cytoplasm. Nucleus. Shuttles between the nucleus and the cytoplasm.

Diseases

• Lupus Erythematosus, Systemic
• Autoimmune Reaction
• Autoimmune Diseases
• Rheumatoid Arthritis
• Arthritis
• Autoimmunity
• Inflammation
• Sclerosis
• Virus Diseases
• Diffuse Scleroderma
• Neoplasms
• Innate Immune Response
• Sjogren's Syndrome

• Malignant Neoplasms
• Fibrosis
• Inflammatory Bowel Diseases
• Dysequilibrium Syndrome
• Diabetes Mellitus
• Crohn Disease
• Colitis

Interacting Proteins

• CREBBP
• MAVS
• RELA
• SGTA

Pathways

• Pathogenesis
• Immune Response
• Localization
• Cell Cycle
• Cytokine Production
• Innate Immune Response
• Secretion
• Cell Cycle Arrest
• Inflammatory Response
• Cell Growth
• Methylation
• Cell Death
• Cell Activation

• Cell Differentiation
• Dna Methylation
• Type I Interferon Production
• Cell Proliferation
• Cellular Localization
• T Cell Activation
• B Cell Activation

PTMs

• Phosphorylation
• Methylation
• Ubiquitination

• Demethylation
• Citrullination
• Acetylation

• Dephosphorylation

Research Areas

• Apoptosis
• Death Receptor Signaling Pathway

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IRF5

Best Uses of the IRF5 Marker

The IRF5 marker is an important regulator of the polarization of M1 macrophages. It regulates transcription of proliferative genes and inhibits the proliferation of macrophages, and is helping to initiate the initial stages of ASC differentiation. Numerous studies have confirmed its significance in cancer research. We will explore the most common uses for the IRF5 marker in this article.

IRF5 is a master regulator for M1 macrophage-polarization

Recent research has revealed that knockdown of the transcription factor IRF5 alters the polarization of macrophages of the human. The knockdown of IRF5 results suppression of expression of M1 inflammation markers, such as IL-1beta. Interestingly, this knockdown did not affect the expression of the M2 genes. These findings highlight the need for further studies and the development of novel treatment strategies.

We have previously shown that IRF5 regulates macrophage polarization M1. Fig. 7a shows the binding site of IRF5. 7a. To stimulate the binding of IRF5 to its promoter regions, we used untreated BMDMs for ChIP treatment as well as LPS treatment. This study also showed that IRF5 was necessary for the polarization of M1 macrophages inside the NEC.

IRF5 interacts with the mPrP receptor within the macrophage's cytosol. In a previous study researchers discovered a peptide, which inhibits IRF5 activity in mPrP-treated macrophages. The peptides bind to IRF5 at a submicromolar level of dissociation constant. We have synthesized 38 peptides with his IRF5-CPPs that are tagged IRF5 to determine whether IRF5 -CPPs interact with IRF5.

In a second study, we discovered that mBSA-infected mice had elevated IRF5 expression. This gene could be a reliable indicator for proinflammatory macrophages in inflammation sites. The research suggests that IRF5 is an important regulator for tracking macrophages in inflammatory conditions. It may play an important role in monitoring inflammatory macrophages when this is the case.

Researchers have confirmed the role that IRF5 played in regulating the M1 macrophage polarization by analyzing levels of this gene in whole cell lysates. They also examined the expression of b-actin as a control to ensure that the effect was not a result of IRF5. The researchers conclude that IRF5 is an essential cell factor that regulates the M1 macrophage polarisation . It can also aid in maturing immune cells.

These findings indicate that IRF5 is a major downstream mediator in the MyD88-dependent TLR signaling process for autoimmune diseases. IRF5-CPPs also inhibit IFNa production by murine pDCs. The major producers of type IIFNa are pDCs. This means that it is possible to use IRF5-CPPs as therapeutic agents to reduce SLE pathogenesis.

It regulates the transcription of pro-apoptotic genes

ST18/NZF3, a newly discovered protein, regulates transcription of proapoptonic genes as well as pro-inflammatory genes. This discovery reveals a previously unknown function. Researchers Yang, Siqueira and Alikhani looked into the regulation of proapoptotic gene expression in fibroblasts. Their research shows that ST18 regulates gene expression and cell death in a cell-like fashion.

ST18 is a tumor cell-specific protein that functions by controlling the transcription of various proapoptotic genes. The gene encodes several important proteins that are involved in apoptosis. It is a member of the forkhead family of transcription factors which include proteins that are similar to Rb or p53 which regulate cell cycle progression. The research in this area has shown ST18 overexpression increases apoptosis.

The expression of ST18 in fibroblasts was investigated using siRNA to test whether ST18 plays an apoptotic part. TNF-a induced a substantial increase in the apoptosis of fibroblasts. However, ST18 siRNA didn't inhibit the basal apoptosis. TNF-a-stimulated cell death was significantly diminished by ST18 siRNA as compared to control siRNA. It is important to note that ST18 siRNA reduced the activity of caspase-3/7 in fibroblasts, which is in line with the silencing data of Fig. 1C.

Recent research has shown that CHOP is a major player in the apoptosis process triggered by ER. In this review, we will review the findings concerning CHOP and its roles in ER stress, microbial infection, and ER-mediated apoptosis. While CHOP is involved in many aspects cell survival however, more research is required to better understand what it does. This is why CHOP is crucial to the apoptotic cascade.

FKHRL1 may work in concert with other factors to inhibit the transcription of genes associated with death. FKHRL1 expression drops when Fas ligand and FKHRL1 are both expressed. Therefore, apoptosis caused by FKHRL1 is reduced when Akt is activated. FKHRL1-mediated suppression through IGF1 is linked to inhibition of PI3K/Akt Signaling.

The Oocyte RNA transcriptome after radiation treatment has been studied. The results show that there is an increase in the expression of the pro-apoptotic and common target genes for p53. However, DNA repair genes do not appear to be upregulated. The expression of genes related to inflammation is also increased when STAT transcription factor is activated by apoptosis. The RNA transcriptome analysis shows that there is a lack of overlap with the transcriptional profile of DNp63a and DNp63a, which indicates distinct regulatory programs.

It is involved in the initial stages of ASC differentiation

In this study, we have discovered that the IRF5 marker contributes to the early stages of ASC differentiation. IRF5 is believed to play a role in cell cycle arrest, apoptosis and the production of cytokines. These findings suggest that IRF5 protein may play a role in the initial stages of ASC differentiation. This is the first study to show that the IRF5 protein plays a role in breast carcinoma.

ASCs express different levels of IRF5 and Blimp1. ASCs that do not express IRF5 are termed Blimp1int and those that express it are known as ASCs that migrate. Blimp1 is a transcriptional regulator that is expressed by B cells during differentiation. It is unclear how Blimp1 helps to ASC differentiation however it is important to note that it is expressed in bone marrow and plasma cells.

The IRF5 protein also regulates DNA damage, which may explain the observed correlation between the loss of IRF5 and increased the degree of invasiveness. We used MCF-12A cell lines transfected with two IRF5 siRNAs and used these cells for the studies. We performed Western analysis using a blot and found that IRF5 expression decreased by 70 percent (normalized to b-actin levels) in the cells. Survival of cells was determined in these cells following exposure to 5-Gy IR as shown by the histograms of representative histograms from three independent studies.

The IRF5 protein, a relatively recent member of the IRF family, has been shown to play a key role in immune response and cell responses to DNA damage. We investigated the expression of IRF5 in breast tissue. We also investigated whether the loss of IRF5 from breast cancer cells can contribute to progress of the disease. It could also contribute to the development of breast cancer.

This study also demonstrated that IRF5 proteins recruit STAT5A and EZH2 that regulate transcription. EZH2 also plays a part in maintaining prePBs' embryonic proliferative condition prior to PC differentiation. We also discovered that the marker IRF5 is responsible for early stages of ASC differentiation in mouse models. The data show that this marker has a direct effect on ASC differentiation.

It stops the proliferation

There is currently no conclusive evidence of whether Boster Bio's IRF5 marker is a powerful anticancer agent. However it is necessary to conduct further research to determine if IRF5 truly is an effective anticancer drug. A new study published in Cell reports that IRF5 knockdown can significantly reduce cell proliferative capacity in a mouse model of prostate cancer. The research seeks to assess the inhibitory properties of IRF5 in various cancer cells.

IRF5 regulates the differentiation and activation of B cells in the human body and cells, and the expression of MYC and the other ASC-associated genes. This is a molecule that can be used to identify drug targets for cancer treatment. Its capability to limit proliferation and induce apoptosis has been proven in a variety of studies, including those conducted in human cancer patients. However this study has a limited application.

The current study showed that IRF5 knockdown significantly decreased plasmablasts and Naive cells. However, knockdown of IRF5 resulted in a decrease in IgD+ B cell proliferation. This is in line with previous findings from mouse models of cancer treatment that showed that cancer-prone B cells tended to increase the number of IgD+ cells. The findings suggest that IRF5 may be involved in the initial breakpoint in self-tolerance.

It is believed that IRF5 regulates the expression of pro-apoptotic genes following DNA damage and death receptor signaling. The IRF5 gene product from Boster Bio inhibits proliferation in human CD19+ B cells. The cells were nucleofected using an anti-IgM-mock antibody and fixed and stained for nuclear DRAQ5 staining. The decrease in cell viability was about 15%.

In the murine model for lupus, IRF5 knockout significantly decreases plasmablast differentiation in naive B cells and ASCs. Alongside the inhibition of proliferation in mice, the removal of IRF5 alleviates the disease in murine lupus models. In addition, the loss of IRF5 causes reduced secretion of pathogenic autoantibodies. Additionally, mice deficient in IRF5 exhibit decreased proliferative capacity.

IRF5 is necessary to produce the proinflammatory phenotype that is present in human monocyte-derived macrophages of GM–CSF. However its levels of expression in murine macrophages have been found to be minimal. Additionally macrophages aren't further stimulated by LPS, which could be related to the availability of activating cofactors. The expression levels of various cytokines indicate the presence of IRF5 in human M-CSF-derived macrophages.