CHI3L1 Antibodies

Chitinase-3-like protein 1 (CHI3L1)

Carbohydrate-binding lectin with a taste for chitin. Has no chitinase activity.

May play a role in tissue remodeling and in the capacity of cells to react to and cope with changes in their surroundings. Plays a role in T-helper cell type 2 (Th2) inflammatory response and IL-13-induced inflammation, regulating allergen sensitization, inflammatory cell apoptosis, dendritic cell accumulation and M2 macrophage differentiation.

Gene Information

Human
Gene Name:	CHI3L1
Uniprot:	P36222
Entrez:	1116

Family

Belongs to:
glycosyl hydrolase 18 family

Alternative Names

AW208766; Brp39; CHI3L1; Chitinase 3 like 1; Chitinase 3-like 1; gp39; HCgp39; YKL-40

Molecular Weight

Mass (kDA):
42.625 kDA

Genomic Context

Human
Location:	1q32.1
Sequence:	1; NC_000001.11 (203178931..203186704, complement)

Tissue Specificity

Present in activated macrophages, articular chondrocytes, synovial cells as well as in liver. Very low or undetectable expression in non-inflammatory colon. Undetectable in muscle tissues, lung, pancreas, mononuclear cells, or fibroblasts.

Subcellular Localizations

Secreted, extracellular space. Cytoplasm. Cytoplasm, perinuclear region. Endoplasmic reticulum.

Diseases

• Inflammation
• Malignant Neoplasms
• Neoplasms
• Arthritis
• Rheumatoid Arthritis
• Degenerative Polyarthritis
• Fibrosis
• Asthma
• Glioblastoma
• Malignant Paraganglionic Neoplasm
• Diabetes Mellitus
• Brain Neoplasms
• Carcinoma

• Glioma
• Malignant Neoplasm Of Breast
• Liver Cirrhosis
• Diabetes Mellitus, Non-insulin-dependent
• Tumor Angiogenesis
• Neoplasm Metastasis
• Hepatitis

Interacting Proteins

• IL13RA2
• LGALS3

Pathways

• Tissue Remodeling
• Pathogenesis
• Secretion
• Angiogenesis
• Cell Proliferation
• Immune Response
• Localization
• Cell Migration
• Cell Cycle
• Cell Death
• Macrophage Activation
• Aging

• Innate Immune Response
• Inflammatory Response
• Cell Adhesion
• Cell Differentiation
• Excretion
• Hypersensitivity
• Chemotaxis

PTMs

• Phosphorylation
• Methylation
• Carboxylation
• Glycosylation

• Cleavage
• Deacetylation
• Citrullination
• Oxidation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CHI3L1

Best Uses Of The CHI3L1 Marker From Boster Bio

If you're thinking of purchasing a CHI3L1 antibody, you could be wondering what it could be employed for. The boster bio CHI3L1 antibodies reacts with human, mouse and rat samples. This product is available through Boster Bio's catalogue and is able to be used in WB applications. Read on to learn more about this antibody and the applications it can serve.

The growth-stimulating protein CHI3L1 is a

A study published in Science Translational Medicine has proven that CHI3L1 may be a growth stimulant that can be used as a tool to predict the treatment of a variety of cancers. Because CHI3L1 expression is sensitive to various types of cancer, it can be utilized as a biomarker for the recurrence of tumors. In addition, the level of expression of CHI3L1 can also be a sign of a patient's prognosis and a possible cancer biomarker.

Interestingly, CHI3L1 has been shown to influence the growth of different types of tumors and cells derived from these tumors. It also has migration-enhancing properties and stimulates angiogenesis and the reorganization process of vascular endothelial cell. The protein works in synergy with the growth-stimulating hormone insulin-like growth factors-1 to enhance synovial cell responses, although it is not fully understood.

While CHI3L1 is a transmembrane-like protein with a glycoprotein-like structure, CHI3L2 does not contain this glycoprotein. It also contains an amino acid sequence that is specific to the heparin binding site, which could explain why it is able to interact with heparin. However, further studies are required to understand the role of CHI3L1 in human cancer cells.

In humans, circulating CHI3L1 has been found to be elevated in patients with inflammation-related diseases like ulcerative colitis, Crohn's disease and asthma. Healthy subjects have a lower circulating CHI3L1, which suggests that CHI3L1 may be an effective indicator of inflammatory activity. Additionally, CHI3L1 is secreted in the form of a soluble substance by mammalian cells of different kinds, including activated neutrophils, macrophages and granulocytes.

The increased expression of CHI3L1 is linked to the development of papillary thyroid cancer. It is also linked to tumor metastasis. This suggests that CHI3L1 could be used as a biomarker to determine prognosis for patients with papillary thyroid cancer. Further research is needed to determine the function of CHI3L1 for the treatment of thyroid cancer.

CHI3L1 is a vital tumor-stimulating protein found in UC. Inflammation plays a significant role in the development of cancers related to UC. Inflammation can increase the expression of CHI3L1 in colon cancer cells. The overexpression of CHI3L1 can cause mutations in susceptibility genes. This can result in an increase in adhesion and invasion of colonic cell lines.

It stimulates macrophages with PD-L1.

A new antibody that targets the chi3L1 marker made by Boster Bio has been created to target the PD-L1 gene to enhance its effect on tumor-associated macrophages that are involved in prostate cancer. This antibody targets the chi3L1 gene and is found in Rab37-specific vesicles on T and macrophages.

The CHI3L1 gene is produced by specialized M2a macrophages and enhances Th2-mediated differentiation of those suffering from inflammatory skin disease. In the course of inflammation both macrophages as well T cells produce the antigen. It can be produced by different types of cells including cancer cells and neutrophils. In addition to stimulating the macrophage PD-L1 pathway, CHI3L1 stimulates the death of tumor-related cells and increases the risk of metastasis.

These results suggest that a combination of monospecific antibodies as well as antibody-drug combinations targeting both CHI3L1 and PD-1 could be effective in the prevention of lung metastasis. Specific antibodies to PD-L1 can be used to block tumor-associated CHI3L1. Combining bispecific and monospecific immunotherapy is an effective treatment option for pulmonary metastasis.

Research conducted with boster Bio's CHI3L1 protein showed that this antibody inhibits tumor associated PD-L1 expression within prostate cancer cells. It not only stimulates T cells, but also blocks the growth of macrophages that are cancer-related. These results are the first to demonstrate that CHI3L1 can inhibit the growth of cancer-related macrophages.

Utilizing the TIRF technique, the researchers observed CHI3L1 signaling near the plasma membrane. When transfected using GFP–CHI3L1 or RFP–Rab37, the signals were quickly observed in RAW264.7 macrophage cell lines. The colocalized signals barely moved in RFP-EV control and GFP-CHI3L1 vector cells.

The NP cells positive for CD206 found in the degenerated discs of rats were also positive for CHI3L1. These cells suggest that the antibody may not target the receptor for PD-1. Further research is needed to differentiate this cell type from macrophages that are truly macrophages. The treatment of disc degeneration might be possible if PD-L1-stimulating antibodies can be produced.

NP cells expressed CHI3L1 and co-localized with IL-13Ra2 receptor. Both proteins are involved in ECM metabolism. The inhibition of IL-13Ra2 via siRNA suppressed chi3L1-induced ECM metabolism. The inhibition by CHI3L1 of both IL-13Ra2 as well as the IL-13Ra2 block ECM metabolism, thus preventing the effects of rCHI3L1.

It blocks the activity of IL-13Ra2

The IL-13Ra2 signalling receptor is that regulates the effects of IL-13 on cells. It plays a role in many crucial biological events. The receptor works with TMEM219 to serve as a partner, and it may play a part in the decoy function. However its role in controlling the HB-EGF pathway is not understood. The study showed Chi3l1 is a factor that inhibits activation of IL-13Ra via a non-targeting mechanism.

CHI3L1 is part of the glycosylhydralase gene family and is highly conserved. Chitinase 3-like-1 (also called YKL-40 in mice and BRP-39 in humans) is produced by a wide range of cells. It is part of a major pathway, controlling cell death and facilitating the process of fibroproliferative repairs.

The human IL-13Ra2 gene was amplified using PCR from lung cDNA. The IL-13Ra2 gene could be amplified by using both reverse and forward primers. A two-hybrid assay using S. cerevisiae was used to determine interactions with other proteins in the cellular. The immune system is co-expressing IL-13Ra2 alongside other cellular proteins.

The multimeric chitosome complex formed by IL-13Ra2 as well as Chi3l1 provides a variety of signalling and response to these molecules. This complex is involved with a number of biological processes, including cancer metastasis, cellular death and TGF-b1 expression. Further research is required to understand the function of Chi3L1 during these processes.

In addition to reducing the IL-13Ra2 pathway, CHI3L1 is a key player in lung injury and oxidant-induced cellular Apoptosis. Chi3L1 (TMEM219) and Chi3L1 (TMEM219) are known to cause increased cell death in response to low doses H2O2, and their suppression increased their sensitivity.

A study that was conducted on mice lacking IL-13Ra2 found that chimeras that contained a knock-out gene were able to display augmented inflammation, signalling, cytokine and IgE responses in response to the IL-13. The results aren't conclusive on the central role of the IL-13Ra2 receptor in controlling inflammation.

The IL-13Ra2 gene has been proven to decrease BAL total protein, which is a measure of lung injury caused by oxidants. The inhibition of IL-13Ra2 reduced the lifespan of mice with inflammatory conditions induced by adenovirus. In contrast, IL-13Ra2 hinders the growth of NFKB. The study also suggests it is unlikely to impact the function of the lungs in healthy mice.

It increases PD-L1 levels during the metastasis of melanoma.

The PDL1 protein plays a key role in the process of melanoma metastasis. The chimeric antigen receptor CHI3L1 was found to increase the amount of this protein in cancer cells. This tumor-independent effect could be utilized to reduce metastasis by targeting PD1-positive cells.

PD-L1 is the key regulator of the polarity M1/M2. By suppressing PDL1, you can increase M1 differentiation. Chi3L1 also enhances PD-1 expression in melanoma metastasisand thereby hindering the growth of tumors. Inflammatory responses may also promote metastasis.

In this study, melanoma tumors were infiltrated into C57BL/6 mice's lungs. Two weeks later, the lung expression of ICP moieties was evaluated. In all, metastasis is caused by increased expression of multiple ICP moieties as well as the PD-L1/PD-2 and PD-L2 axis.

Interaction between PD-L1 and Chi3L1 is responsible for the inhibition of melanoma metastasis in mice. Antibodies that target both Chi3l1 and the PD-1 inhibitory mechanism inhibit metastasis dose-dependent way. Combination therapies that include both anti-PD-1 or anti -Chi3l1 are promising to treat melanoma.

Activation of RLH blocks CHI3L1 stimulation. It is not yet known why CHI3L1 blocks PD1 expression in Melanoma cell lines. It is important to remember that RLH may block the induction of that PD-L1. Chi3L1 activates Wnt/bcatenin signaling and could be involved in the inhibition of metastasis to melanoma.

Chi3L1 has been proven to increase the activity of the other ICP moieties that is a remarkable result in melanomas. The simultaneous targeting of Chi3l1 as well as PD-L1 is a promising therapeutic strategy to combat the pulmonary metastasis. Chi3L1 is a tumor-suppressor and is essential to the PD-1-mediated anti-tumor response.

The current study found that CHI3L1 stimulation in melanoma metastase prone mice increased the levels of expression of several other tumor suppressors, including perforin, granzyme , and the tumor-suppressor PTEN. These results are consistent in other reports. Chi3L1 is a promising treatment for stimulation in Melanoma Metastasis.