Tenascin Antibodies

Tenascin (TNC)

Extracellular matrix protein implicated in advice of migrating neurons in addition to axons during development, synaptic plasticity in addition to neuronal regeneration. Promotes neurite outgrowth from cortical neurons grown on a monolayer of astrocytes.

Ligand for integrins alpha-8/beta-1, alpha-9/beta-1, alpha-V/beta-3 and alpha-V/beta-6. In tumors, stimulates angiogenesis by elongation, migration and regeneration of endothelial cells (PubMed:19884327).

Gene Information

Human
Gene Name:	TNC
Uniprot:	P24821
Entrez:	3371

Family

Belongs to:
tenascin family

Alternative Names

150-225; Cytotactin; Glioma-associated-extracellular matrix antigen; GMEM; GP 150-225; hexabrachion (tenascin C, cytotactin); hexabrachion (tenascin); Hexabrachion; HXB; HXBcytotactin; JI; MGC167029; Myotendinous antigen; neuronectin; Tenascin C; Tenascin J1; tenascin; tenascin-C isoform 14/AD1/16; Tenascin-C; TNC; TN-C; TNGP

Molecular Weight

Mass (kDA):
240.853 kDA

Genomic Context

Human
Location:	9q33.1
Sequence:	9; NC_000009.12 (115019575..115118244, complement)

Subcellular Localizations

Secreted, extracellular space, extracellular matrix.

Diseases

• Neoplasms
• Malignant Neoplasms
• Migraine Disorders
• Headache
• Tissue Adhesions
• Inflammation
• Graft-vs-host Disease
• Pain
• Cardiomyopathies
• Muscle Rigidity
• Neoplasm Metastasis
• Leukemia
• Malignant Paraganglionic Neoplasm

• Cell Invasion
• Hematologic Neoplasms
• Myocardial Infarction
• Carcinoma
• Muscle Twitch
• Observation Of Neuromuscular Block
• Acute Gvh Disease

Interacting Proteins

• COL5A1
• TLR4

Pathways

• Muscle Contraction
• Regulation Of Muscle Contraction
• Cardiac Muscle Contraction
• Skeletal Muscle Contraction
• Pathogenesis
• Regeneration
• Striated Muscle Contraction
• Wound Healing
• Cell Adhesion
• Cell Migration
• Localization
• Sensitization
• Cell Proliferation

• Transport
• Proteolysis
• Tissue Remodeling
• Cell Differentiation
• T Cell Differentiation
• Angiogenesis
• Photosynthesis

PTMs

• Phosphorylation
• Cleavage
• Reduction
• Oxidation
• Acetylation
• Nitration

• Dephosphorylation
• Carboxylation
• Glutathionylation
• Phosphorothioation
• Glycosylation
• Deamidation

Research Areas

• Breast Cancer
• Cancer
• Extracellular Matrix
• Neuroscience
• Prostate Cancer

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

Best Uses Of The TNC Marker In Boster Bio

There are a lot of questions that arise when conducting experiments using the Boster Bio, and these guides will help you figure out the best method to optimize your experiment. Boster Bio optimization guides can aid you in understanding your results to help you make informed decisions. Additionally, every researcher will encounter some type of trouble in their research. In order to minimize the sources of error, employ Boster Bio troubleshooting guidelines.

Anti-Tenascin-C

Boster Bio's Anti-Tenascin Marker is a glycoprotein encoded in the TNC gene. It is found in the extracellular matrix in various tissues and in restricted areas of the central nervous system. It is the main member of the Tenascin gene family and plays an important role in cell signaling. It is abundantly present in the developing tendons, bone cartilage, cartilage and other tissues. It regulates cell proliferation and mobility, and is released in response to various environmental stimuli, such as trauma or inflammation.

Six subunits comprise the tenascin C molecule, each with multiple domains. The amino-terminal interchain crosslinking molecule is followed by a sequence of fibronectin type III repeats. A fibronectin-like repeat is also located at the C-terminal region of the Tenascin C molecule. In chicken and human samples, there are three different variants of the tenascin C gene.

The Anti-Tenascin-ADC and TN-190 are the two most well known tenascin-C molecule and were tested in conjunction with fibronectin. CEF-TN slowed cell attachment by 80%, while both TN-ADC as well as TN-190 had one effect. Both tenascin C and fibronectin inhibited cell attachment to a specific type of cell in a manner similar that the fibronectin effect.

Anti-Tenascin antibody detects elevated levels of tenascin-C within the various tissues of the body that include the skin and brain, heart, and other body tissue. Its expression is regulated by various genes in the body including the brain and the heart. It is found in the bones, blood, and muscles. When cells interact with tenascin it forms clusters of microspikes in the fascia.

Anti-LAMP1

Anti-LAMP1 antibodies target the TNC, an extracellular matrix protein that is non-structural. This protein has multiple roles, including in morphogenesis, tissue remodelling, and in cellular responses. There is growing evidence that TNC is involved in the development of OA. TNC levels are high in many OA patients. However, it is not clear if this is the main cause. TNC has been implicated in OA pathogenesis through studies of various tissues.

There are numerous suppliers who sell anti-LAMP1 antibodies. Antibodies against the Lysosomal Assoc. Membran Protein 1 are effective tools in the field of cancer research. These antibodies are also referred to as CD107a, LAMPA, and may have orthologs. This study highlights the importance of this marker, which has been extensively utilized in the diagnosis of cancer. Antibodies that target LAMP1 can be used to identify tumors and autophagic pathways.

A rabbit polyclonal antigen against LC3 and anti-LAMP1 was employed to determine whether the fusion proteins were cross-reactive. The anti-LAMP1 mAbs also were used for western blot analysis. The antibodies were detected through Western Blot and flow cytometry. The data obtained with these antibodies were validated by immunohistochemistry.

The Anti-LAMP1 antibodies that were used in this study detected LC3-II-positive cells in vitro. They were associated with an increase in autophagy. The results were published in the supplement to Fig. S2C on Rheumatology online. These studies provide fresh information on the function of TNC markers in RA research. This article will assist you to find an anti-LAMP1 antimouse antibody.

Anti-FN

Numerous recent studies have revealed the positive predictive value of Anti-FN uses of the TNC marker. FN and TNC are crucial indicators for EMT which is crucial for the spread of cancerous cells. FN is upregulated within the stroma of head and neck cancer. TNC levels that are high TNC in tumors are associated with an increase in cervical metastases, aswell in a rise in mortality specific to disease. A recent study found that there is a positive correlation between stromal FN levels and the early stage of OSTCC.

In the present study, we used multiple parallel line raster scans to create the distribution maps. The lines that rasterized were offset 65 mm. The entire map area was ablated by an average size of 14 8mm x 14. A single sample took four hours to complete. We injected 7.5 mg/kg NWs into mice that had tumors in their tail vein. Then, we conducted cardiac perfusion with 20 ml PBS/DMEM. We then removed the control and tumor organs. The NW injection was administered 15 minutes prior to when the blocking antibodies were administered.

Anti-FN uses of the TNC marker were previously discovered as being effective in the detection of human squamous cell carcinomas. These tumors can be resistant to conventional treatments. Patients with these tumors are usually resistant to conventional treatments. We have been able to identify TNC antibodies in these patients with high sensitivity. We are developing anti-FN therapies based on these findings. This research is a crucial step towards developing effective treatments for head and neck cancers.

We are now able not just to target FNEDB, but also the TNC. We have discovered a bispecific protein (PL1) that recognizes both TNC-C as well as FN-EDB. This peptide can be used to deliver imaging agents and therapeutics to tumors. This research is thrilling! The future is bright! The future is bright in this field.

Anti-RA

This study assessed serum TNC levels between patients with RA and UC who had suffered from arthrocentesis. The levels were higher for patients with UC and CD as well as patients who had a larger disease extension had higher TNC levels. Patients suffering from UC or RA with colon involvement or penetrating behaviors had TNC levels in their serum that were higher. However, statistically, there were no significant differences between patients with UC or those without disease extension.

Subjects suffering from RA have higher rates of cit-TNC-specific T cell than those with HC. T cells that are activated by Cit-TNC also express CD38, which is an activation marker on CD4+ memory T cells. Furthermore, ciTNC specific T cell responses are strong. Anti-RA usage of the TNC marker can enhance the efficacy of immunotherapy.

The TNC-C molecule, an extracellular protein that is soluble and has proinflammatory properties is a molecules. Its antigen-recognition abilities and ability to stimulate T cells were discovered through a systematic process of discovery. The results showed that CD4+ T cells with specificity for cit-TNC epitopes exhibited an increase in the synovial fluid as well as in peripheral blood of RA patients. Two epitopes CRP (C-reactive protein) and IL-1b were recognized by antibodies.

Cit-TNC17 and cit -TNC56 peptides can be recognized by the antibodies in RA subjects. They also enhance T cell responses to TNC. In addition to these benefits However, there are some limitations. However, these findings are still important and deserve further investigation. The TNC marker will continue to be an essential component of RA immunotherapy. However, more research is required to prove its efficacy in clinical situations.

Anti-OA

TNC is a possible therapeutic target for OA. Studies have revealed that antiTNC antibodies inhibit TNC expression in vascular smooth muscle cells. In Japan the drug hydroxyfasudil has been extensively used to treat cardiovascular diseases following SAH. Despite these promising results, anti-TNC therapies have not been tested in clinical situations. Further studies are required to determine the optimal treatment strategy for this biomarker.

The most popular anti-OA uses for this biomarker are aimed towards defining the OA phenotype and identifying its molecular constituents. The last year, the primary focus was on cartilage-driven phenotypes which are caused due to the MMP CRPM. These findings can be used to guide clinical trials for patients with OA. Further research on OA could identify novel biomarkers that could help with a new treatment strategy.

Studies have shown that antiOA drugs can inhibit the TNC marker through regulation of CTL function. TNC also influences T lymphocyte proliferation and adhesion. It is also believed to increase the growth of tumor cells and reduce the immune system against tumors. These results suggest that TNC could have therapeutic applications in OA. TNC is a novel antiOA marker. However clinical trials are required to verify its efficacy.

Tissue-dependent proteomic analyses were used to study human knee OA synovial fluid. It showed that the TNC marker could be a good candidate for an OA biomarker. This study is the first to detect the presence of proteins in articular synovial fluids from knee patients OA. However, the results are limited since many of the proteins in OA synovial fluids are unknown intra-articular tissues.