Product: GRO alpha Antibody
Catalog: AF5403
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Mol.Wt.: 11 kD; 11kD(Calculated).
Uniprot: P09341
RRID: AB_2837887

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Clonality:
Polyclonal
Specificity:
GRO alpha Antibody detects endogenous levels of total GRO alpha.
RRID:
AB_2837887
Cite Format: Affinity Biosciences Cat# AF5403, RRID:AB_2837887.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

C-X-C motif chemokine 1; Chemokine (C-X-C motif) ligand 1 (melanoma growth stimulating activity, alpha); chemokine (C-X-C motif) ligand 1; CINC-1; CXCL1; Cytokine-induced neutrophil chemoattractant 1; Fibroblast secretory protein; Fsp; Gro 1; Gro A; Gro; GRO protein, alpha; GRO-alpha(1-73); GRO-alpha(6-73); Gro1; GRO1 oncogene (melanoma growth stimulating activity, alpha); GRO1 oncogene (melanoma growth-stimulating activity); Gro1 oncogene; GROa; GROA_HUMAN; Growth-regulated alpha protein; KC; KC chemokine, mouse, homolog of; melanoma growth stimulatory activity alpha; Melanoma growth stimulatory activity; Melanoma growth stimulatory activity, alpha; MGSA alpha; MGSA; MGSA-a; N51; NAP-3; NAP3; Neutrophil-activating protein 3; Platelet-derived growth factor-inducible protein KC; Scyb 1; Scyb1; Secretory protein N51; Small inducible cytokine subfamily B, member 1;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
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.
Sequence:
MARAALSAAPSNPRLLRVALLLLLLVAAGRRAAGASVATELRCQCLQTLQGIHPKNIQSVNVKSPGPHCAQTEVIATLKNGRKACLNPASPIVKKIIEKMLNSDKSN

Research Backgrounds

Function:

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.

PTMs:

N-terminal processed forms GRO-alpha(4-73), GRO-alpha(5-73) and GRO-alpha(6-73) are produced by proteolytic cleavage after secretion from peripheral blood monocytes.

Subcellular Location:

Secreted.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

Belongs to the intercrine alpha (chemokine CxC) family.

Research Fields

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

References

1). Ren QC et al. Total flavonoids from sea buckthorn ameliorates lipopolysaccharide/cigarette smoke-induced airway inflammation. Phytother Res 2019 Jun 17 (PubMed: 31209984) [IF=6.388]

Application: IHC    Species: mouse    Sample: lung

FIGURE 7 |Total flavonoids from sea buckthorn fruit (TFSB) treatment suppressed the expression of cytokines, chemokines, and MUC5AC in bronchial tissues in lipopolysaccharide/cigarette smoke extract (LPS/CS)‐exposed mice. After LPS/CS exposure, mice were treated with TFSB (100, 200, and 500 mg/kg) or dexamethasone (0.25 mg/kg). After treatment of TFSB, lung tissues were used to detect the expression of (a) IL‐1β,(b) IL‐6, (c) COX2, (d) MUC5AC, and (e) CXCL1 through immunohistochemical method. (f) The quantitative results of the expression of IL‐1β, IL‐6,COX2, MUC5AC, and CXCL1 were shown, respectively. Bar = 50 μm. *p < .05, **p < .01, ***p < .001, ****p < .0001, versus LPS/CS alone, n = 4

2). Wang S et al. XIAOPI formula inhibits breast cancer stem cells via suppressing TAMs/CXCL1 pathway. Front Pharmacol 2019 Nov 15;10:1371. (PubMed: 31803057) [IF=5.810]

Application: WB    Species: human and mouse    Sample: TAMs

FIGURE 3 | XIAOPI formula (XPS) inhibits M2 phenotype polarization, C-X-C motif chemokine ligand 1 (CXCL1) expression and secretion of tumor-associated macrophages (TAMs).(D–E) Western blot and QPCR results further verified that XIAOPI formula treatment for 48 h could dramatically inhibit CXCL1 protein expression levels (D) and CXCL1 mRNA transcription levels (E) in both human and mouse TAMs. (F) Double luciferase reporter gene assay suggested that XPS treatment for 48 h could suppress the promoter activity of CXCL1 gene in Raw264.7-derived TAMs. All values are presented as the mean ± SD, n = 3, **P < 0.05.

Application: IF/ICC    Species: mouse    Sample: macrophages

FIGURE 5 | XIAOPI formula (XPS) suppresses breast tumor growth and breast cancer stem cells (CSCs) activity in vivo. (D–E) XPS administration significantly decreased the infiltration degree of macrophages as well as their M2 phenotype polarization and C-X-C motif chemokine ligand 1 (CXCL1) expression in the 4T1-Luc xenografts in vivo. n = 3.

3). Jiao J et al. A Mouse Model of Damp-Heat Syndrome in Traditional Chinese Medicine and Its Impact on Pancreatic Tumor Growth. Front Oncol 2022 Jul 25;12:947238. (PubMed: 35957897) [IF=5.738]

4). Zheng Y et al. XIAOPI formula inhibits the pre-metastatic niche formation in breast cancer via suppressing TAMs/CXCL1 signaling. Cell Commun Signal 2020 Mar 26;18(1):48 (PubMed: 32213179) [IF=5.712]

Application: WB    Species: mouse    Sample: M2 phenotype RAW264.7 cells

Fig. 1| XIAOPI formula suppresses the polarization of M2 macrophages and CXCL1 expression.e XIAOPI formula dose-dependently inhibited expression of CXCL1 in M2 phenotype RAW264.7 cells. (The results were obtained from triplicate experiments and were represented as mean values ± SD.,*P < 0.05, **P < 0.01 as compared with control, ##P < 0.01, comparison between three time points of 24 h, 48 h, and 72 h)

5). Li J et al. Aiduqing formula inhibits breast cancer metastasis by suppressing TAM/CXCL1-induced Treg differentiation and infiltration. Cell Commun Signal 2021 Aug 30;19(1):89. (PubMed: 34461944) [IF=5.712]

Application: WB    Species: Mice    Sample: breast tumor tissues

Fig. 2 ADQ inhibits M2 phenotype polarization and CXCL1 secretion by TAMs in vitro and in vivo. a Flow cytometry assay was conducted to investigate the effect of ADQ treatment (0.7 or 1.4 g/kg/day) on TAM infiltration and polarization within the TME of breast tumors. b The expression levels of CD206 (red) and CXCL1 (green) in breast tumor tissues were detected by the tissue immunofluorescence assay. Scale bar = 5 μm. c 40 ng/ml IL-4 and IL-13 were used to induce the transformation of Raw264.7 macrophages into M2-like macrophages (TAMs). Their phenotype validation was conducted by flow cytometry. d The cell viability changes of TAMs when treated with ADQ (20–200 μg/ml) for 12–48 h were detected using the CCK-8 assay. e–f The phenotype changes of Raw264.7-derived TAMs when treated with 20–200 μg/ml ADQ for 24 h were detected by flow cytometry. G–i Raw264.7-derived TAMs were treated with ADQ (20–200 μg/ml) for 24 h. The protein expression, secretion as well as mRNA transcription levels of CXCL1 in Raw264.7-derived TAMs were detected by Western blot, ELISA, and qPCR assays, respectively. j Raw264.7-derived TAMs were treated with ADQ (20–200 μg/Ml) for 24 h. The promoter activity changes of CXCL1 gene in Raw264.7-derived TAMs were detected by the double luciferase reporter gene assay. N = 3. *p < 0.05. **p < 0.01

Application: IF/ICC    Species: Mice    Sample: breast tumor tissues

Fig. 2 ADQ inhibits M2 phenotype polarization and CXCL1 secretion by TAMs in vitro and in vivo. a Flow cytometry assay was conducted to investigate the effect of ADQ treatment (0.7 or 1.4 g/kg/day) on TAM infiltration and polarization within the TME of breast tumors. b The expression levels of CD206 (red) and CXCL1 (green) in breast tumor tissues were detected by the tissue immunofluorescence assay. Scale bar = 5 μm. c 40 ng/ml IL-4 and IL-13 were used to induce the transformation of Raw264.7 macrophages into M2-like macrophages (TAMs). Their phenotype validation was conducted by flow cytometry. d The cell viability changes of TAMs when treated with ADQ (20–200 μg/ml) for 12–48 h were detected using the CCK-8 assay. e–f The phenotype changes of Raw264.7-derived TAMs when treated with 20–200 μg/ml ADQ for 24 h were detected by flow cytometry. G–i Raw264.7-derived TAMs were treated with ADQ (20–200 μg/ml) for 24 h. The protein expression, secretion as well as mRNA transcription levels of CXCL1 in Raw264.7-derived TAMs were detected by Western blot, ELISA, and qPCR assays, respectively. j Raw264.7-derived TAMs were treated with ADQ (20–200 μg/Ml) for 24 h. The promoter activity changes of CXCL1 gene in Raw264.7-derived TAMs were detected by the double luciferase reporter gene assay. N = 3. *p < 0.05. **p < 0.01

6). Li C et al. The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection. Invest Ophthalmol Vis Sci 2020 Feb 7;61(2):25 (PubMed: 32084267) [IF=4.925]

Application: WB    Species: mouse    Sample: corneas

FIGURE 4.| Effect of autophagy on PMN recruitment and morphology. (A-C) The mRNA levels of CXCL-1 in corneas of C57BL/6 mice after 3-MA, CQ, or rapamycin treatment at 3 days p.i.; (D-F) The protein level of CXCL-1 in corneas of C57BL/6 mice after 3-MA, CQ, or rapamycin treatment at 3 days p.

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Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.