CXCL12 Antibodies

Stromal cell-derived factor 1 (CXCL12)

Chemoattractant active on T-lymphocytes and monocytes but not neutrophils. Activates the C-X-C chemokine receptor CXCR4 to cause a rapid and transient rise in the level of intracellular calcium ions and chemotaxis.

Binding to cell surface proteoglycans seems to inhibit formation of SDF-1-alpha(3-67) and thus to preserve activity on local websites. Also binds to atypical chemokine receptor ACKR3, which triggers the beta-arrestin pathway and acts as a scavenger receptor for SDF-1.

Gene Information

Human
Gene Name:	CXCL12
Uniprot:	P48061
Entrez:	6387

Family

Belongs to:
intercrine alpha (chemokine CxC) family

Alternative Names

chemokine (C-X-C motif) ligand 12; C-X-C motif chemokine 12; CXCL12; hIRH; hSDF-1; Intercrine reduced in hepatomas; IRH; PBSF; PBSFSDF-1a; Pre-B cell growth-stimulating factor; SCYB12; SDF1; SDF-1; SDF1A; SDF1B; SDF1SDF-1b; stromal cell-derived factor 1; TLSF; TLSF-a; TLSF-b; TPAR1

Molecular Weight

Mass (kDA):
10.666 kDA

Genomic Context

Human
Location:	10q11.21
Sequence:	10; NC_000010.11 (44292088..44385097, complement)

Tissue Specificity

Isoform Alpha and isoform Beta are ubiquitously expressed, with highest levels detected in liver, pancreas and spleen. Isoform Gamma is mainly expressed in heart, with weak expression detected in several other tissues. Isoform Delta, isoform Epsilon and isoform Theta have highest expression levels in pancreas, with lower levels detected in heart, kidney, liver and spleen.

Subcellular Localizations

Secreted.

Diseases

• Malignant Neoplasms
• Neoplasms
• Neoplasm Metastasis
• Tissue Adhesions
• Hiv Infections
• Inflammation
• Immunologic Deficiency Syndromes
• Tumor Angiogenesis
• Cell Invasion
• Carcinoma
• Leukemia
• Pathologic Neovascularization

• Malignant Neoplasm Of Breast
• Malignant Paraganglionic Neoplasm
• Mammary Neoplasms
• Neoplasm Invasiveness
• Nervousness
• Acquired Immunodeficiency Syndrome

Interacting Proteins

• CCL11
• CCL13
• CCL20
• CCL21
• CCL25

• CCL26
• CCL28
• CCL5
• CXCL10
• CXCL11

• CXCL14
• CXCL17
• CXCL2
• CXCL6
• CXCL9

• PF4
• PF4V1
• XCL1
• XCL2

Pathways

• Chemotaxis
• Cell Migration
• Angiogenesis
• Pathogenesis
• Secretion
• Cell Adhesion
• Cell Proliferation
• Localization
• Regeneration
• Immune Response
• Cell Growth
• Cell Chemotaxis
• Cell Motility

• Cell Death
• Vasculogenesis
• T Cell Migration
• Lymphocyte Migration
• Wound Healing
• Cell Activation
• Cell Cycle

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Glycosylation
• Acetylation
• Ubiquitination
• Demethylation
• Dephosphorylation
• Prenylation
• Biotinylation

• Reduction
• Oxidation
• Sumoylation
• Phosphorothioation
• Citrullination
• Acylation
• Deamidation
• Amination
• Palmitoylation
• Deglycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CXCL12

Best Uses Of The CXCL12 Marker From Boster Bio

This article will explain how CXCL12 regulates OPC proliferation and migration to improve the remyelination process. We will also cover the relationship between CXCL9, CXCL12, and how they affect remyelination and predict infection. We'll also look at how CXCL12 stimulates B cell activity during infections.

CXCL12 encourages B cells to be active in anti-infective illnesses

CXCL12 is a chemokine that promotes the activity of B cells in fighting infections. It is responsible for the antiviral properties of B cells. B cells can be polarized between light and darkness. Normally, CXCL12 promotes the migration of B cells into the light zone, and HMGB1 inhibits the migration of B cells in the dark zone.

CXCL12 activates B cells and increases expression of two anti-inflammatory receptors, pCREB (previously pTAOK). Anti-IgM-mediated stimulation of B cells increased the expression of these molecules. Combining anti IgM and CXCL12 increases the activity of B-cells in anti-infective diseases, but not their cytotoxic ability.

Exogenous CXCL12 increases the expression of ADAM10 from wild-type B cell lines. Immunohistochemistry and flow cytometry analysis confirmed that CXCL12 increases plasma membrane ADAM10 expression. CXCL12 also increases the expression CD23 on transitional B cell lines, while CD81 expression is decreased. The upregulation of ADAM10 on T0/T1 cells is compromised by loss of Gai proteins and signaling.

CXCL12 also stimulates normal transitional B cells. The effect of inhibiting Gai nucleotide exchange blocked ADAM10 upregulation after cross-linking with the antigen receptor. Gai promotes the maturation of and activity of B cells transitional. Notch2 signaling also boosts MZ-B cell development. This study demonstrates the importance of Gai in anti-infective immunity.

Gai plays an important role in the regulation and function of immune cells. The vast majority of B cells are activated in the PPs and undergo immunoglobulin class switch recombination from IgM to IgA. IgA+-expressing B cells then localize in the small intestinale to the lamina propria. There they transform into IgA secreting plasma cells.

CXCL12 stimulates B cell activity and has a significant effect upon TB's inflammatory responses. These immune responses are dependent on balanced regulation of the host's innate and adaptive defenses. CXCL12, which plays a detrimental role in promoting neutrophilic swelling, is also implicated in TB pathogenesis. CXCL12 is therefore essential for the development of TB.

CXCL12 encourages OPC migration to increase remyelination

CXCL12 expression is linked to OPC numbers in mice deficient in TNFR2. Astrocytes provide vital support to neurons by providing trophic, metabolic and other functions in the CNS. Their role in CNS regeneration and repair remains unclear. Reactive astrocytes inhibit OPC differentiation in vitro and reduce remyelination.

Recent studies have identified a number of potential targets for myelination promotion in multiple sclerosis patients. CXCL12, a chemotherapy that promotes migration in oligodendrocyte (OPC) progenitor cell cells (chemokine), is one of these targets. These cells are essential to remyelination damage axons. CXCL12 was found to promote OPCs' differentiation into myelinating Ooligodendrocytes.

Although it is not clear how CXCR4 mediates OPC maturation, recent research shows that this molecule activates PI3K/AKT/MEK/ERK pathways. CXCL12 also promotes OPC migration in chronically demyelinated CC. CXCL12 promotes OPC movement via the TNFR2 signaling pathway.

It may take longer to restore depleted OPC than you expected. Gene therapy may require multiple gene therapy lentiviruses that express multiple chemokines. These chemokines can be used to stimulate OPC recruitment, proliferation differentiation, migration, and/or differentiation. Ex-vivo gene therapy for the treatment of MS may be used to replenish astrocytes in depleted glial cells. Also, increasing CXCL12 expression can improve myelin expression within depleted MS astrocytes.

The expression of CXCL12 promotes neuro/oligodendrocyte differentiation in EAE-recovered mice. CXCL12 may promote myelin repair and endogenous neurogenesis, according to some studies. It is also associated with enhanced neurogenesis in MS-like mice's brains. CXCL12 led to an increase in the number of NG2+ OPCs as well as CCR4+ DCX+ NCS in a mouse-model study.

The study authors discovered that CXCL12 concentrations were high in brain tissue even after mice had stopped exhibiting EAE symptoms. After recovery, CXCL12 levels in mice were significantly higher than in naive animals. CXCL12 was also persistent in the mice that were subject to the study. This was despite the fact that CNS inflammation had declined. During recovery, however CD3+ cells as well as MAC2+ cells were reduced.

CXCL9 predicts infections

The antigen, CXCL9, from Boster Bio is monoclonal and reacts with the mouse CXCL9 chemokine. CXCL9 is part of the CXC Chemokine Family and is expressed by many cell types. Boster Bio CXCL9 antibody is known to increase chemokine by activating integrins and altering cytoskeletal structures. They may also serve as a marker for intraodal TCM peripherization.

Although the human CXCL9 gene can be found in the genome, its receptor is unknown. The gene is closely linked to the expression of a wide range of cell types, even non-malignant ones. Cells that express CXCL9 have the ability to attract and activate CD4+ T cells. CXCL9 expression in cells promotes immune response and inflammation. CXCL9-mediated inflammation is increased by inflammation of the cell membrane.

CXCL9 detection was achieved by infecting ME180 cells with HSV-2 for 24 hours. The supernatant was collected from the cells and centrifuged to remove any debris. The supernatants were used to quantify human CXCL9 using a BD Cytometric Bead Array Human Soluble Protein Flexset Kit. The kit includes 50 mL beads as well as a PE conjugated detection anti-body. After the sample was dried, it was analysed for CXCL9 production.

Previous studies revealed that CXCL9/CXCL10 expression was higher in cervical tissues from HSV-2-infected mice. CXCL9, CXCR3 ligands were shown to play a key role in HSV-2 infection control and CD4+ T-cell migration. The role of CXCL9 is still unknown.

CXCL12 regulates OPC proliferation

The OPC migration process is influenced by the MEK/ERK/AKT pathways and PI3K/AKT pathways. We used inhibitors of these pathways, U1026 and LY294002, to study the effects of CXCL12 on OPC proliferation and migration. Both inhibitors significantly decreased OPC migration. These results also support CXCL12's hypothesis that it regulates OPC proliferation by inhibiting certain pathways.

CXCL12, a stromal cell-derived factor, is an important mediator for multiple cell migration. CXCL12 is a factor that regulates OPC proliferation, differentiation, and improves remyelination. The mechanism by which CXCL12-induced OPC Migration is effected remains unclear. This review will examine the current literature to determine CXCL12’s role in OPC differentiation and migration.

Previous research has shown that Rac1 (and CXCL12) are key factors in the osteoinductive and chemotactic activities OPCs. CXCL12 antagonists block Rac1 and decrease the number of OPCs recruited in the PGIS model. However, these pathways can still be inhibited by inhibitors. They have not been shown to suppress pathological new bone formation. Our findings suggest that CXCL12 may act as a novel therapeutic target for osteoporosis.

In addition to regulating OPC proliferation and migration, CXCL12 also controls myelination in the CNS. It regulates OPC migration via the MEK/ERK pathway. These findings have important implications to the development of therapies for remyelination. They also reveal the therapeutic value of CXCL12 when treating demyelinating illnesses. There are several potential benefits of this treatment.

In a mouse model of demyelination, CPZ induces OPC apoptosis and inhibits differentiation. Cuprizone also increases CXCR4 level in immature OPCs. Continual consumption results in apoptosis, chronic demyelination, and apoptosis. These results indicate that CXCL12/CXCR4 signalling could be an important factor for OPC differentiation.

First, we isolated primary rat OPCs in order to study the role of CXCL12 on OPC proliferation. The cells that were isolated showed typical OPC morphology. They also expressed markers specific to OPCs. However, they did not have markers specific for mature oligodendrocytes. We also differentiated these cells in mature oligodendrocytes and confirmed that the isolated cells were OPCs.