C-X-C motif chemokine 6 Antibodies

C-X-C motif chemokine 6 (CXCL6)

Chemotactic for neutrophil granulocytes. Signals through binding and activation of its receptors (CXCR1 and CXCR2).

Besides its chemotactic and angiogenic properties, it has strong antibacterial activity against Gram-positive and Gram- negative bacteria (90-fold-higher when compared to CXCL5 and CXCL7). .

Gene Information

Human
Gene Name:	CXCL6
Uniprot:	P80162
Entrez:	6372

Family

Belongs to:
intercrine alpha (chemokine CxC) family

Alternative Names

chemokine (C-X-C motif) ligand 6 (granulocyte chemotactic protein 2); Chemokine alpha 3; CKA-3Granulocyte chemotactic protein 2; CXCL6; GCP-2; GCP2member 6 (granulocytechemotactic protein 2); GCP-2Small-inducible cytokine B6; Small inducible cytokine subfamily B (Cys-X-Cys), member b

Molecular Weight

Mass (kDA):
11.897 kDA

Genomic Context

Human
Location:	4q13.3
Sequence:	4; NC_000004.12 (73836678..73838760)

Subcellular Localizations

Secreted.

Diseases

• Inflammation
• Neoplasms
• Tumor Angiogenesis
• Malignant Neoplasms
• Inflammatory Response
• Carcinoma
• Cholangiocarcinoma
• Neoplasm Metastasis
• Tissue Adhesions
• Pathologic Neovascularization
• Arthritis
• Osteosarcoma

• Liver Carcinoma
• Cell Invasion
• Innate Immune Response
• Rheumatoid Arthritis
• Fibrosis
• Chronic Inflammation
• Liver Neoplasms

Interacting Proteins

• CCL5
• CXCL12
• PF4

Pathways

• Chemotaxis
• Angiogenesis
• Pathogenesis
• Secretion
• Inflammatory Response
• Neutrophil Chemotaxis
• Immune Response
• Cell Adhesion
• Chemokine Production
• Cell Proliferation
• Cell Migration
• Innate Immune Response
• Neutrophil Activation

• Coagulation
• Leukocyte Migration
• Localization
• Chemokine Secretion
• Regeneration
• Leukocyte Chemotaxis
• Monocyte Chemotaxis

PTMs

• Cleavage
• Phosphorylation

• Demethylation
• Glycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CXCL6

Best Uses Of The CXCL6 Marker

You might have heard about the CXCL6 marker, but do you know how it is used? It is an anti–CCL5 antibody, or metabolite, that neutralizes CCL5. This molecule is used in research to determine the function of the arteriolar niche, which has been altered by malignant remodeling. This marker is produced by neutralizing antibodies to CCL5. This marker is also accessible to all Boster scientists worldwide.

CXCL6 Marker

CXCL6 expression is upregulated in BM cells in AML as a compensatory response. This was to increase EC viability and improve angiogenesis. However, the long-term hypoxia damage prevented autocrine CXCL6 production, leading to irreversible EC depletion and the collapse of the arteriolar niche.

CXCL6 was used to stain bone-marrow neutrophils. CXCL6 was found in healthy resting neutrophils at a concentration equal to 0.4+0.07ng per 106 cells. CXCL6 levels in neutrophils were measured using the enzyme-linked antibodysorbent assay.

RNA-sequencing data has been used to examine the role of CXCL6 within various cellular processes. The resulting gene expression profiles were analyzed by GSEA. GSEA was performed with GEO data sets, accession ID GSE28221.

The CXCL6 protein promotes the expression and activation of fibrosis related factors and JAK/STAT3 signals. It has the potential to be a candidate biomarker and a therapeutic target. CXCL6 neutralization has been shown to reduce the risk of fibrosis and increase lung collagen. If you're curious about CXCL6 and its clinical utility, keep reading!

Arginine Metabolite

A new study has revealed a new aspect to arginine metabolism: homoarginine. These findings have greater implications for metabolic system, including vascular biology. This study will be Boster Bio's first to report the Arginine Metabolite. Learn more about this compound. What is it, and how does it impact bone remodeling? This study is published by Circulation.

Arginine is a key component in the translation of protein. The urea cycle allows cells to synthesize the amino acid, which allows them use this nutrient. However, the body has a limit on how much arginine it can store in its cells. Arginine gets then transported into the cells' nucleus. When cells are depleted of arginine, the body must import arginine from the extracellular space. In addition, Arginine is converted by urea cycle enzymes.

When cells have a low concentration of arginine, the resulting protein level should decrease. The polyarginine region also contains 20 arginine amino acids, which allows for a more targeted response to intracellular Arginine levels. This results in slower translations of the downstream reporter protein. This decrease is an issue with the ArgSen based model, but the overall pattern for sensor fluorescence remains constant.

Arginine Metabolite in BoSTER Bio includes the protein known as Arginine Oxidase. This enzyme is responsible to neutralize antibodies that react with arginaine. Those antibodies are called metabolites. These antibodies are monoclonal, as well as polyclonal. They are accessible to all Boster scientists. The enzyme's target site will help identify the specific protein and its role in metabolizing arginine.

The time travel theory has many parallels in arginine metabolism. In a fictional novel, "The Time Traveler" is a main character who accidentally steps on a butterfly. Later, he travels backwards in time and finds that irreversible modifications have occurred. The same principle applies in arginine metabolism. Even subtle changes in one metabolite can have profound consequences in distantly related metabolites.

Blocking CCR5 Neutralization

This study describes an antibiotic that can be used to treat tumors. It was created from the discovery that CCR5 neutralization using the CXCL6 marker could inhibit immune response. Intraakines (or intraabodies) are single-chain intracellular antibodies that bind CCR5. The latter trap CCR5 in the cell to stop its surface expression and recycle. This anti-tumor drug can be used to inflame the skin.

CCR5 plays an important role in the progression and prevention of human cancer. This seven transmembrane GPCR is normally found only in the immune cells. However, breast cancer is one of many malignancies that overexpress CCR5. CCR5+ breast cancer patients are more than half of those with triple-negative disease. CCR5-positive tumors are associated with poor prognosis.

CCR5 can be stopped by blocking CXCL6's interactions with other chemokine receptacles. The anti-tumor drug PDK1 may block its action. CCR5 receptors are also binded by CXCL6 markers. This allows them to bind to these targets while not affecting T cell activation. This anti-tumor drug proved effective in a clinical trial. It may also have other applications.

LERONLIMAT (leronlimab), blocks CCR5 and inhibits calcium releasing in response to ligands. The drug also blocks tumor-promoting signaling, including calcium-induced cells migration. CCR5 neutralization can be blocked with the CXCL6 marker, which can increase the effectiveness of treatment and increase survival rates for patients with cancer.

CCR5 expression doesn't correlate with clinical parameters in any significant way, but a large number of HIV-infected people have a significantly lower CD4+ T cell count. This suggests that the decrease in CD4+ T cell count may be due to a different immune mechanism. Although there isn't enough evidence to support CCR5-mediated neutralization in CMI as a cause, this drug has the potential of influencing the development of immune responses in human patients.

Anti-CCR5Ab recognizes the conformational epitope for the first external loop of receptor and inhibits the immune reaction of the virus. This prevents HIV entry to the cell. Filypin and nocodazole can be used as inhibitors to prevent internalization. Blocking the viral immune system by increasing cell-mediated HIV infection and inhibiting CCR5 nullization with inhibitoryRNAs or ribozymes.

Reversing malignant remodeling in the arteriolar niche

In the context of AML, the circulating level of CXCL6 increased to compensate for extensive severe hypoxia in the BM. CXCL6 regulation was initiated to promote EC viability, and angiogenesis. The hypoxia-induced damage over time prevented autocrine CXCL6 from being produced. CXCL6 is a novel strategy to restore the arteriole nidus. Further investigation is needed to understand the precise mechanism and timing of CXCL6 production in vivo.

Reversing malignant remodeling of the arterial niche with the CXCL6 marker is a promising approach for treating a variety of cancers. AML is characterized as a number of thin-walled arterioles located in the endosteum. In contrast, the arteriolar and mid-brain arterioles are abundant and thick-walled.

While brief periods of severe Hypoxia can increase HSC viability, prolonged severe Hypoxia reduces MSCs in the arteriolar space, which accelerates the development and transformation of LSCs into AML. Despite the implications for vascular structure, function, and the presence of CXCL6 markers, there was no direct correlation with improved hematopoietic performance in AML patients.