TNFSF12 Antibodies

Tumor necrosis factor ligand superfamily member 12 (TNFSF12)

Binds to FN14 and possibly also to TNRFSF12/APO3.

Weak inducer of apoptosis in certain cell types.

Mediates NF-kappa-B activation. Promotes angiogenesis and the proliferation of endothelial cells.

Gene Information

Human
Gene Name:	TNFSF12
Uniprot:	O43508
Entrez:	8742

Family

Belongs to:
tumor necrosis factor family

Alternative Names

APO3 ligand; APO3LMGC20669; DR3LGTWEAKAPO3/DR3 ligand; MGC129581; TNF-related weak inducer of apoptosis; TNFSF12; tumor necrosis factor (ligand) superfamily, member 12; tumor necrosis factor ligand superfamily member 12; TWEAK

Molecular Weight

Mass (kDA):
27.216 kDA

Genomic Context

Human
Location:	17p13.1
Sequence:	17; NC_000017.11 (7549058..7557881)

Tissue Specificity

Highly expressed in adult heart, pancreas, skeletal muscle, brain, colon, small intestine, lung, ovary, prostate, spleen, lymph node, appendix and peripheral blood lymphocytes. Low expression in kidney, testis, liver, placenta, thymus and bone marrow. Also detected in fetal kidney, liver, lung and brain.

Subcellular Localizations

Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 12, secreted form]: Secreted.; [Isoform TWE-PRIL]: Cell membrane; Single-pass membrane protein.

Diseases

• Inflammation
• Tumor Angiogenesis
• Malignant Neoplasms
• Neoplasms
• Lupus Erythematosus, Systemic
• Kidney Diseases
• Atherosclerosis
• Nephritis
• Rheumatoid Arthritis
• Lupus Nephritis
• Arthritis
• Pathologic Neovascularization
• Autoimmune Reaction

• Cardiovascular Diseases
• Hyperplasia
• Fibrosis
• Ischemia
• Injury To Kidney
• Muscular Atrophy
• Acute Kidney Injury

Interacting Proteins

• DICER1
• TNFRSF12A

Pathways

• Pathogenesis
• Angiogenesis
• Cell Death
• Cell Proliferation
• Secretion
• Cell Growth
• Inflammatory Response
• Regeneration
• Muscle Atrophy
• Cytokine Production
• Tissue Remodeling
• Skeletal Muscle Atrophy
• Cell Migration

• Cell Differentiation
• Cell Adhesion
• Chemokine Production
• Osteoblast Differentiation
• Mating
• Ovulation
• Aging

PTMs

• Phosphorylation
• Cleavage

• Ubiquitination
• Deacetylation

• Methylation

Research Areas

• Angiogenesis
• Apoptosis
• Cancer
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TNFSF12

Best Uses Of The TNFSF12 Marker

This article outlines the history of Boster Bio: the company, the product, and the various applications. In addition, it outlines GO analysis of microglial clusters 2 and 19 and the CVID-associated genes. Finally, it discusses the various clinical applications. This information is applicable to scientists in any field worldwide. This article is written with the help of Boster scientists.

Boster's history

The author's first product was developed in 1993 and earned the nickname "he who converts science in the lavatory." Over the next few decades, Boster would create several different products, including IHC kits and hundreds of primary antibodies. By the late 1990s, Boster was the largest catalog antibody company in China. Boster's technology helped him develop the PicoKine(tm) proprietary ELISA platform, which delivers highly sensitive ELISA kits.

The text is divided into three main parts, each focusing on a different aspect of the history of slavery in the American South. Boster introduces each section by discussing the history of a fugitive slave, Tom Wilson, who was later retold by abolitionists and other potential buyers. In this way, Boster connects the two stories: abolitionist propaganda and the exhibition of fugitive slaves to prospective buyers. Boster also offers a number of examples of the abolitionists' stance against slavery and the stories of the disabled fugitive slaves.

GO analysis of microglial clusters 2 and 19

In a GO analysis of microglial clusters 2, 19, and 20, we found that the genes within these groups mainly reflect the activities of different types of microglia. We also found that microglia lose their resting signature upon activation and acquire an acute one, indicating that they have distinct functions. This study reveals the complex interactions between microglial clusters, which may be important for the diagnosis of various neurodegenerative and inflammatory conditions.

We then calculated differential module eigengene expression using the App-Ps1 dataset, and compared these with the other submodules. For each module, we performed a Kruskall-Wallis test to determine the significance of the differences between conditions. We also tested for overlaps between modules using the Fisher's exact test. Finally, we calculated the ME of the modules in WebGestalt, using the KEGG and GO analysis.

Gene ontology terms that were enriched in both datasets related to developmental stages. For example, PU.1 and IRF8 were significantly expressed in pre and adult microglia, respectively. These genes are crucial for the ontogeny and development of murine microglia, and their overexpression reveals that the cells are critical for brain development and homeostasis. Further, they were associated with a wide range of functions in the brain.

Using the KEGG pathway and Gene Ontology enrichment analyses, we identified genes that are related to microglial processes. These genes were assigned to modules according to their KEGG pathway membership. Hub genes were categorized as either acute or primed. In terms of functional roles, they were found to be 'hub' genes in the acute and primed microglia consensus networks. These genes were also highly connected, and their expression pattern revealed a striking similarity between the two clusters.

GO analysis of CVID-associated genes

The GO analysis of CVID-associated genes provides a list of shared GO terms that are significantly enriched for the corresponding gene sets. This list also includes the frequency of each term in the sample and background, expected p-value, and over and underrepresentation of the GO terms. In addition, the results of the analysis provide details of the criteria used to identify genes. The top five GO terms are summarized in Table 3.

The TNFRSF13B gene mutation is associated with about 8% of CVID cases and is found in normal blood donors as well as unaffected siblings. Other genes associated with CVID include NFKB1, but not in all affected family members. This disease is also associated with recessive genes such as LRBA, but its occurrence is rare in most families. Therefore, it is important to understand the underlying biology of CVID and identify novel targets for targeted therapies.

The MHC gene(s) associated with IgAD and CVID are related to similar functions in the human body. This suggests that the two diseases share a common genetic defect. In addition, the GO analysis of CVID-associated genes will uncover the role of novel genes in the development of the disease. While the analysis suggests that CVID-associated genes are associated with a broad set of disease-related pathways, it does not rule out the existence of additional genes that may contribute to the pathogenesis of IgAD.

Approximately 20% of CVID cases have a familial history. While some are hereditary, most of these cases remain unexplained. One recent study linked CVID to DNA methylation. This suggests that DNA methylation is a central component of CVID. GO analysis of CVID-associated genes shows a high number of gene regulatory pathways involved in the disease. One can also look at the association between genes and disease severity.

Clinical applications

TNFSF12 is a member of the tumor necrosis factor superfamily. It is also known as TWEAK, a ligand of fibroblast growth factor inducible 14. TNFSF12 is activated by the NF-kB signaling pathway. Overexpression of TNFSF12 is associated with poor treatment outcomes in gastric, breast, and prostate cancer. TNFSF12 promotes invasiveness in prostate, breast, and glioma cells. Blocking TWEAK may inhibit metastasis in breast cancer.

The study also found that TNFSF12 was associated with a decreased risk of intracranial bleeding in ischemic stroke patients. The findings are consistent with previous studies, which show that TNFSF12 is a potentially valuable biomarker in ischemic stroke. The circulating levels of SCARA5 and F11 may have therapeutic roles in other disorders. However, more studies are needed to determine whether these markers are viable targets for drug development.

A recent study conducted by Dom et al used the SOMAscan proteomics platform to measure TNFSF12 and renal protective proteins in blood plasma. The T2D cohort they studied had a short duration of disease and normal eGFR. However, their BMI was higher than that of the controls. The researchers confirmed the protective relationship between TNFSF12 and renal function in an independent group of 294 type 1 diabetics. The researchers also found that TNFSF12 was elevated in the plasmas of diabetic children with no kidney complications.

Fn14 is also associated with the progression of multiple human cancers. The Oncomine database showed that TWEAK and Fn14 were highly expressed in multiple cancer cell lines, except for bladder, kidney, and liver. However, TWEAK was expressed in lung cancer samples in six independent datasets. This result was consistent across all six datasets. These findings suggest that TWEAK and Fn14 may be correlated in lung cancer.

High-affinity primary antibodies

Human TNFSF12 is a highly expressed molecule expressed in a variety of tissues and cancer cells. It is a member of the TNFRSF family and plays a role in tumor development and progression. It is associated with apoptosis and promotes tumor invasiveness. The primary antibodies raised against TNFSF12 are available in various isotypes and species.

Human antibody polyclonal antigens are readily available and have been developed in laboratories around the world. Affinity antibodies are purified using peptide antigens to produce high affinity and specificity. They are highly specific and conform to the internationally recognized definition of a monospecific antibody. They can be used in research studies in animal and human cells. These antibodies have been validated using samples from many species and have passed through protein array and knockout validation.

The TNFSF12 protein is expressed by the immune system in the blood and is involved in several processes in the body. High-affinity primary antibodies against this protein can detect TNFSF12 protein in both healthy and diseased cells. The TNFSF12 marker is expressed in most human tissues and can be detected with the help of CF(tm) dyes. However, in the case of TNFSF12, CF(tm) dyes are not as specific as primary antibodies.

The study of TNFSF proteins has grown immensely over the past thirty years. In addition to being a central part of inflammatory and autoimmune diseases, TNFSF proteins play a crucial role in the regulation of cellular differentiation, survival, and programmed death. Dysregulation of TNFSF/TNFRSF proteins is linked to several inflammatory and autoimmune diseases. For this reason, high-affinity primary antibodies against the TNFSF12 marker have been developed and are available in clinical trials.