CXCR1 Antibodies

C-X-C chemokine receptor type 1 (CXCR1)

Receptor to interleukin-8, which is a powerful neutrophils chemotactic factor. Binding of IL-8 to the receptor causes activation of neutrophils.

This response is mediated via a G-protein that trigger a phosphatidylinositol-calcium second messenger system. This receptor binds to IL-8 using a high affinity and to MGSA (GRO) with a low affinity.

Gene Information

Human
Gene Name:	CXCR1
Uniprot:	P25024
Entrez:	3577

Family

Belongs to:
G-protein coupled receptor 1 family

Alternative Names

CD128; CD181 antigen; CD181; CDw128aC-C; chemokine (C-X-C motif) receptor 1; CKR-1; CMKAR1; C-X-C chemokine receptor type 1; CXCR1; CXC-R1; CXCR-1; High affinity interleukin-8 receptor A; IL-8 RA; IL-8 receptor type 1; IL-8R A; IL8R1; IL8RA; IL8RAC-C-CKR-1; IL8RBA; interleukin 8 receptor, alpha; interleukin-8 receptor type 1; interleukin-8 receptor type A

Molecular Weight

Mass (kDA):
39.791 kDA

Genomic Context

Human
Location:	2q35
Sequence:	2; NC_000002.12 (218162841..218166962, complement)

Subcellular Localizations

Cell membrane; Multi-pass membrane protein.

Diseases

• Inflammation
• Neoplasms
• Malignant Neoplasms
• Tumor Angiogenesis
• Tissue Adhesions
• Neoplasm Metastasis
• Cholangiocarcinoma
• Infective Disorder
• Lung Diseases
• Pathologic Neovascularization
• Inflammatory Response
• Malignant Paraganglionic Neoplasm

• Melanoma
• Chronic Obstructive Airway Disease
• Arthritis
• Lung Diseases, Obstructive
• Carcinoma
• Asthma
• Rheumatoid Arthritis

Pathways

• Chemotaxis
• Pathogenesis
• Angiogenesis
• Secretion
• Cell Migration
• Inflammatory Response
• Neutrophil Chemotaxis
• Cell Proliferation
• Immune Response
• Neutrophil Activation
• Receptor Internalization
• Leukocyte Migration
• Wound Healing

• Phagocytosis
• Chemokine Production
• Localization
• Cell Growth
• Exocytosis
• Cell Activation
• Cell Chemotaxis

PTMs

• Phosphorylation
• Cleavage
• Formylation

• Glycosylation
• Methylation
• Amidation

• Dephosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CXCR1

Best Uses For CXCR1 Antibodies

What is CXCR1? CSCs use this C-XC motif chemokine receptor as a key marker. This receptor is also a target to CXCR1/2 inhibiters. This article will discuss the use CXCR1 in research. We will also discuss how to identify this molecule in the body. We'll also discuss how to identify the protein and explore the best uses for CXCR1 antibodies.

CXCR1 is a CX-C motif chemokine receiver

CXCR1 is 4149bp long. It contains two exons, and the coding regions. There are 165 known SNPs in this gene, many of which are associated with disease states. CXCR1 & CXCR2 share 76% amino acids identity and the same chromosome 2q34-35. This suggests gene duplication due to the close proximity of these genes. Primer extension analysis also revealed two start sites for the CXCR1 gene. This is consistent with the existence of two transcripts within neutrophils.

Neutrophils express a CXC motif chemotactic receptor mainly on neutrophils. CXCL2 can be produced by neutrophils as a major chemokine. It binds directly to the atypical chemokine ACKR1. This chemokine receptor is expressed by the endothelial junctions of post-capillary venules and guides neutrophils to their extravasation sites. CXCL1 mediates neutrophil adhesion, intraluminal crawling and pericyte inflamation.

These C-X chemokine receptors for the C-XC motif chemotaxis chemokine chemokine receptors may not be the only chemokine receptors. However, there are many potential uses for C-XC peptides. In addition to their application in cancer and aging, C-X-C chemokines may be effective vaccine adjuvants and aid wound healing.

CC chemokines play a role in the development and maintenance of cancerous cells. They are involved in leukocyte migration, secondary lymphoid development, and mediating CC chemokines. These chemokines also can be produced by non-immune, such endothelial, cells. CXCL2 and infection-related chemicals such as CXCL2 have been shown to cause cancer cell production of ROS.

CXCR1 is a candidate gene that causes urinary tract infection. It was first identified in the development and progression of the disease as a possible gene. Mice with the mIL-8Rh mutation developed severe renal scattering and acute pielonephritis. In addition, Lundstedt et al. Lundstedt and colleagues also found two sequence variants which impair CXCR1 expression. They then observed decreased levels CXCR1 protein among UTI patients. Arenberger et.al. also found CXCR1 hyperexpression in patients suffering from psoriasis.

The structural features of the monomer bound complex of CXCL8 are almost identical, according to Xray crystallography. Both chemokine receptors bind chemokines in a 'two-step' mechanism, and CXCR1 is a C-X-C motif cheokine receptor

It is a symbol of CSCs

Researchers recently discovered that CXCR1 was a marker for cancer-stem cells (CSCs) through a study. CXCR1 inhibition could be a new therapeutic option for cancer treatment. They examined tumor cells from patients with high CXCR1 or low levels. The results showed that these patients had a longer median OS.

Studies have not yet revealed specific markers to identify different molecular subtypes. Recent studies have shown CXCR2 to be a suitable CSC marker for TNBC. CXCR2 can be expressed by both TNBC and cancer cells. It may be used in future studies to determine which CSCs cause breast cancer. The National Natural Sciences Foundation of China (81372506) & the Sichuan Society of Medicine (116042) are acknowledged by the authors. YW and LT carried out experiments and collected data. MJ and DC analyzed and drafted manuscripts. FL was responsible for the supervision of the project and the review of the manuscript. All authors approved the final content and gave their approval.

Researchers previously discovered CD133, a novel marker in cancer stem cells. Anti-CD133 antibodies have been shown to eradicate cancer cells in vivo. The mechanism of CD133 in normal tissues remains unknown. However, bi-specific antibodies targeting CD133 are able to activate T cells and induce the cytotoxic response against cancer cells. CXCR1 might also be a CSC marker.

CXCR1 was associated with the presence of CSCs (in PDAC), but further studies are needed in order to determine its role. CXCR1 was found in 23 percent of nonSP cells and only eight% of SP cells. In a separate study, researchers also identified a subtype called breast CSCs.

It is also believed that the protein plays an important role for drug resistance in cancer-stem cells. Researchers have found that MSCs secrete the cytokine IL-1 and the pro-stem cytokine IL-6. Anti-IL-6 antibodies block IL-6 receptors and inhibit IL-6 production, thereby preventing the proliferation of cancer stem cells. CSCs are responsible both for tumor heterogeneity, and therapeutic resistance. It is important to understand why they become resistant to therapeutic agents.

It is a target area for CXCR1/2 inhibiters

CXCRs are the receptors for chemokines CXCL8/IL-8. Both have a critical N terminal motif that mediates interactions of chemoattractant compounds. CXCRs are expressed on cell surfaces by different cell types. These receptors are combined with CXCR1 or b-arrestin2.

P. M. Murphy provided the ORF of human CXCR1 and PCR-amplified it from pCEP4 plasmid. Two-step PCR was used for the generation of mutant receptors using swapped amino acids 133 & 132. Double-stranded sequencing DNA was used to confirm the nucleotide sequences. Repertaxin showed similar inhibitory activity to PMN when used against CXCR2-transfected C1.2-cells.

CXCR1 plays an important role in several types of cancer. We examined the effects of stable CXCR1 overexpression or knockdown on various aspects of cancer. MKN45 and BGC823 cells were transfected with shRNA and pIRES2-ZsGreen1-CXCR1. We evaluated the phenotypes of malignant behavior and their expression using flow cytometry, wound heal assays, CXCR1/2 signaling chemicals, and flow cytometry.

Furthermore, CXCR1 inhibition inhibits the proliferation of tumor cells and angiogenesis. This study also suggests that CXCR1 inhibition inhibits the proliferation of CSC. Further studies are needed before we can confirm that CXCR1 inhibition inclines CSC. CXCR1 inhibitors reduce angiogenesis, and inhibit the expression of cell cycle regulators in cancer-cell cells. The results of the current study reveal that cancer tumors express CXCR1 (and CXCL8).

In a placebo-controlled, randomized clinical trial, we discovered that reparixin inhibited CXCR1+ cell recruitment in malignant melanoma. The results of this study indicate that CXCR1/2 inhibition inhibits tumor cells proliferation and suppresses ALDH+ cell growth. Patients with metastatic TNBC are currently undergoing clinical trials for the inhibitor.

It has also been investigated how reparixin works. It inhibits the binding CXCR1 to IL-8. Reparixin was also shown to inhibit CXCR1 to CXCR1 binding by increasing IL-8 activity. Its mechanism works differently from the orthosteric CXCR1/2 inhibitor.

It is a mark for CSCs

CSC markers have been identified with a variety molecules. CD44 and CD133 are the most commonly used CSC markers. Both markers have prognostic value, but it is not known if they play a role in cancer treatment. Other molecules found in cancer cells may also be potential CSC markers. Below are the most commonly used CSC markers as well as their roles within cancer.

CSCs have opened the door for new therapeutic approaches. However, there are still challenges. Researchers must also identify new CSC markers. They also need to better understand and determine the regulation of these markers so that they can be applied to new therapeutic approaches. Although the development and application of tools and techniques for targeting cancer stem cells is still in the early stages, this research is still very much in its infancy. Eventually, however, it is expected that CSC-targeting therapies will become a major focus in drug development.

CSC markers are identified through extensive research into the biology and behavior of cancer cells. CSC differentiation may be influenced by aldehyde-dehydrogenase 1. This is a detoxifying enzyme. Aldehyde hydrogenase-1 (ALDh2) positive cells were able produce tumors from mice's mammary oil pads. This indicates they have the properties that CSCs. The isolation of CSCs has been successful in several cancer types, including melanoma, prostate, bone sarcoma, head and neck cancer, and ovarian cancer.

In cancer, CSCs develop from the plasticity of the tumor and its stem cells. These cancer cells can be either derived from an adult stem cell, or a slightly differentiated precursor cell. Researchers have discovered that CSC-specific TFs overexpression is linked to cancer stem cell pathology. Ultimately, CSCs serve as the core reservoir of cancer cells and are implicated in intrinsic resistance models.