CXCL1 Antibodies

Growth-regulated alpha protein (CXCL1)

Has chemotactic activity for neutrophils. May play a role in inflammation and exerts its effects on endothelial cells in an autocrine fashion.

In vitro, the processed forms GRO- alpha(4-73), GRO-alpha(5-73) and GRO-alpha(6-73) show a 30-fold higher chemotactic activity. .

Gene Information

Human
Gene Name:	CXCL1
Uniprot:	P09341
Entrez:	2919

Family

Belongs to:
intercrine alpha (chemokine CxC) family

Alternative Names

CINC1; CINC-1; CXCL1; GRO alpha; KC; MGSA-alpha

Molecular Weight

Mass (kDA):
11.301 kDA

Genomic Context

Human
Location:	4q13.3
Sequence:	4; NC_000004.12 (73869393..73871308)

Subcellular Localizations

Secreted.

Diseases

• Inflammation
• Tissue Adhesions
• Neoplasms
• Inflammatory Response
• Malignant Neoplasms
• Melanoma
• Pneumonia
• Tumor Angiogenesis
• Lung Injury
• Ischemia
• Edema
• Neoplasm Metastasis
• Infective Disorder

• Carcinoma
• Reperfusion Injury
• Arthritis
• Innate Immune Response
• Lung Diseases
• Cholangiocarcinoma
• Nervousness

Pathways

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

• Wound Healing
• Localization
• Cell Death
• Cell Growth
• Neutrophil Activation
• Chemokine Secretion
• Phagocytosis

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Acetylation
• Oxidation
• Dephosphorylation
• Amidation
• Iodination

• Nitration
• Reduction
• Glycosylation
• Sumoylation
• Nitrosylation
• Carboxylation
• Ribosylation
• Ubiquitination

• Biotinylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CXCL1

Best Uses of the CXCL1 Marker by Boster Bio

Boster Bio's Anti CD34 Antibody is well-known however, what is their CXCL1 Marker. You'll soon discover the mechanism behind this marker and how to use it correctly. This article will describe the mechanism of this antibody and how it can be used to study TNF-a-induced CXCL1 for your own experiments.

Boster Bio Anti-CD34 Antibody

Boster Bio's Anti-CD34 Antibody was specifically designed to conduct research in human stem cell research. The antibody reacts to EPCs from rats and mice, and contains 5 mg BSA. The antibody is composed of the 74-92aa sequence. Scientists can submit their results to receive product credits. The company is a partner in research projects across all disciplines including academic research.

Boster Bio CXCL1 Marker

Boster Bio CXCL1 Marker is accessible to researchers from all over the globe. This product has been validated for Western Blotting, Immunohistochemistry, and ELISA. Additionally the Boster Bio anti-CD34 antibody is compatible with Human, Mouse, and Rat. This article will discuss the best uses of Boster Bio's CXCL1 marker.

Boster Bio TNF-a-induced CXCL1 production

CXCL1/CXCL5 induced by TNF was blocked in mice by LIX/CXCL5 (and reparixin). The peptides triggered CXCR2 receptors in mast cells and macrophages and stimulated the production of tumor necrosis factors-alpha. After being challenged with the KC/CXCL1 and LIX/CXCL5 peptide were analyzed for 4 hours.

Antibodies against CXCL1 are available at several websites including Boster Bio. Boster Bio Anti–GRO alpha/CXCL1 antibody, a human antibody, is available. It can be stored at -20°C and -80°F for up to six months. It contains five milligrams BSA and 0.05m Thimerosal. It recognizes human GRO alpha protein and the KMLNSDKSN sequence, and can be used for both qualitative and quantitative studies. If you are conducting a functional study you must purchase a blocking peptide in order to neutralize the antibody.

TNF-a is produced by KC/CXCL1 or the LIX/CXCL5. TNF-a plays a crucial role in neutrophil recruitment. Therefore, the Boster Bio TNF-a-induced CXCL1 and LIX/CXCL5 antibody block these two pathways. The researchers concluded that blocking TNF-a-induced CXCL1 and LIF inhibit neutrophil recruitment in inflammatory mice.

The immunemodulator LQ inhibits BCP-induced CXCL1 production. LQ also has antinociceptive properties. It blocks the activation of astrocytes in the spinal cord, inhibiting the increase in CXCL1 and LIF. LQ also blocks the upregulation of CXCR2 receptors in astrocytes. In a mouse model for osteoporosis the anti-inflammatory effects of Boster Bio-induced CXCL1 have been observed.

Production of CXCL1 by TNF-a-induced

TNF-a activates CC cell PI3K/Akt pathways , and activates p65. This nuclear receptor binds to CXCL10 promoter. Additionally, TNF-a stimulates Akt and PI3K, two other pathways that regulate cancer cell migration and EMT. These findings suggest that TNF-a-induced CXCL1 produces CC cell migration and EMT.

TNF-a induces the expression of CXCR3 and CXCL10 in CC cells and in a concentration-dependent manner. Induction of CXCL10 was particularly evident at a concentration of 20 ng/ml but the effect as TNF-a concentration was increased. The treatment of CC cells with Boster Bio's TNF-a-induced CXCL1 significantly increased CXCR3 mRNA and protein expression as well as transcriptional activity, in both SW480 and SW620 cells.

We also tested the effects of TNF-a on CXCL4 secretion in monocytic human monocytic cell lines. We used a THP-1 commercial X Blue cell line that was treated with LPS and TNF-a at the dose and time. THP-1 cells were transformed into macrophages by PMA after 24 hours. We then examined the secreted CCL4 levels in the cell supernat.

TNF-a triggers CCL4 expression in human monocytes via an activation process known as NF-kB, SAPK/JNK signaling and. This study offers new insights into the role that TNF-a plays in the inflammation response and in the development of disease. Boster Bio's TNFa-induced CXCL1 production could be the next best thing.

TNF-a stimulation also induces the phosphorylation of two proteins involved in NF-kB signaling. These proteins are activated by TNF-a when it is bound to them. Additionally, TNF-a triggers nuclear translocation p65 and IkB cytoplasmic degradation which, in turn, trigger CXCL1 production.

In addition to the effects of TNF-a-induced CXCL10 in astrocytes, the transfection with the p65-Luc promoter plasmid was found to significantly suppress mechanical allodynia as well as luciferase gene expression. Furthermore, co-transfection of p65-Luc and Gap27-Luc promoter plasmids decreased both CXCL10 and luciferase gene activation.