CXCL5 + CXCL6 Antibody [P8L5] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IF1:1000 FCM1:500

Application
WB, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
12 kDa 12 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
CXCL5 + CXCL6 Antibody [P8L5] detects endogenous levels of total CXCL5 and CXCL6 protein.

Clone
P8L5

Synonym(s)
ENA78, SCYB5, CXCL5, C-X-C motif chemokine 5, ENA-78(1-78), GCP2, SCYB6, CXCL6, C-X-C motif chemokine 6, Chemokine alpha 3, Granulocyte chemotactic protein 2, Small-inducible cytokine B6, CKA-3, GCP-2

Background
CXCL5 and CXCL6 are ELR‑positive CXC chemokines that share the conserved CXC motif and N‑terminal glutamate–leucine–arginine sequence and act as secreted ligands for the neutrophil chemokine receptor CXCR2, with CXCL6 also engaging CXCR1 in some contexts. Their small chemokine fold, formed by an N‑terminal region, three antiparallel β‑strands, and a C‑terminal α‑helix, positions the ELR segment and key receptor‑contact residues to trigger G protein–coupled signaling when they bind CXCR2 on neutrophils and other responsive cells. Receptor engagement activates Gαi‑dependent pathways, causes calcium influx, and stimulates PI3K, ERK, and p38 MAPK cascades, which together promote integrin activation, chemotaxis, degranulation, oxidative burst, and release of additional inflammatory mediators that reinforce innate immune responses. CXCL5 is produced by epithelial cells, stromal cells, and tumor‑associated myeloid cells under the control of inflammatory cytokines and microbial or damage signals, and its expression aligns with strong neutrophil recruitment and with induction of matrix metalloproteinases such as MMP‑2 and MMP‑9 that remodel tissue barriers and extracellular matrix. CXCL6 is induced by interleukins and other inflammatory stimuli in stromal and tumor compartments and contributes to neutrophil‑rich inflammation, fibrosis, and reparative responses, and also appears in pro‑angiogenic secretomes where it supports endothelial migration and tube formation through CXCR1/2 signaling. Elevated CXCL5 and CXCL6 in synovial fluid and tissue are reported in inflammatory arthritides, where their presence is associated with neutrophil infiltration, synovial angiogenesis, and markers of persistent synovitis and joint damage. Across multiple solid tumors, CXCL5 expression correlates with higher grade and poorer prognosis, and mechanistic work links CXCL5–CXCR2 signaling to activation of ERK/Elk‑1/Snail and AKT/GSK3β/β‑catenin pathways, promotion of epithelial–mesenchymal transition, and recruitment of myeloid cells that support immunosuppressive, pro‑angiogenic microenvironments.

Background

CXCL5 and CXCL6 are ELR‑positive CXC chemokines that share the conserved CXC motif and N‑terminal glutamate–leucine–arginine sequence and act as secreted ligands for the neutrophil chemokine receptor CXCR2, with CXCL6 also engaging CXCR1 in some contexts. Their small chemokine fold, formed by an N‑terminal region, three antiparallel β‑strands, and a C‑terminal α‑helix, positions the ELR segment and key receptor‑contact residues to trigger G protein–coupled signaling when they bind CXCR2 on neutrophils and other responsive cells. Receptor engagement activates Gαi‑dependent pathways, causes calcium influx, and stimulates PI3K, ERK, and p38 MAPK cascades, which together promote integrin activation, chemotaxis, degranulation, oxidative burst, and release of additional inflammatory mediators that reinforce innate immune responses. CXCL5 is produced by epithelial cells, stromal cells, and tumor‑associated myeloid cells under the control of inflammatory cytokines and microbial or damage signals, and its expression aligns with strong neutrophil recruitment and with induction of matrix metalloproteinases such as MMP‑2 and MMP‑9 that remodel tissue barriers and extracellular matrix. CXCL6 is induced by interleukins and other inflammatory stimuli in stromal and tumor compartments and contributes to neutrophil‑rich inflammation, fibrosis, and reparative responses, and also appears in pro‑angiogenic secretomes where it supports endothelial migration and tube formation through CXCR1/2 signaling. Elevated CXCL5 and CXCL6 in synovial fluid and tissue are reported in inflammatory arthritides, where their presence is associated with neutrophil infiltration, synovial angiogenesis, and markers of persistent synovitis and joint damage. Across multiple solid tumors, CXCL5 expression correlates with higher grade and poorer prognosis, and mechanistic work links CXCL5–CXCR2 signaling to activation of ERK/Elk‑1/Snail and AKT/GSK3β/β‑catenin pathways, promotion of epithelial–mesenchymal transition, and recruitment of myeloid cells that support immunosuppressive, pro‑angiogenic microenvironments.

References
https://pubmed.ncbi.nlm.nih.gov/37612429/ https://pubmed.ncbi.nlm.nih.gov/35978824/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%