PA5-86508
antibody from Invitrogen Antibodies
Targeting: CXCL1
FSP, GRO1, GROa, MGSA, MGSA-a, NAP-3, SCYB1
Antibody data
- Antibody Data
- Antigen structure
- References [4]
- Comments [0]
- Validations
- Western blot [2]
- Immunocytochemistry [2]
- Immunohistochemistry [1]
- Other assay [3]
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- Product number
- PA5-86508 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- CXCL1 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Reactivity
- Human, Mouse, Rat
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 µL
- Concentration
- 1 mg/mL
- Storage
- Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.
Submitted references Pharmacological perturbation of CXCL1 signaling alleviates neuropathogenesis in a model of HEVA71 infection.
Monovalent antibody-conjugated lipid-polymer nanohybrids for active targeting to desmoglein 3 of keratinocytes to attenuate psoriasiform inflammation.
Involvement of CXCL1/CXCR2 During Microglia Activation Following Inflammation-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Rats.
CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway.
Gunaseelan S, Ariffin MZ, Khanna S, Ooi MH, Perera D, Chu JJH, Chua JJE
Nature communications 2022 Feb 16;13(1):890
Nature communications 2022 Feb 16;13(1):890
Monovalent antibody-conjugated lipid-polymer nanohybrids for active targeting to desmoglein 3 of keratinocytes to attenuate psoriasiform inflammation.
Lin ZC, Hwang TL, Huang TH, Tahara K, Trousil J, Fang JY
Theranostics 2021;11(10):4567-4584
Theranostics 2021;11(10):4567-4584
Involvement of CXCL1/CXCR2 During Microglia Activation Following Inflammation-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Rats.
Serdar M, Kempe K, Herrmann R, Picard D, Remke M, Herz J, Bendix I, Felderhoff-Müser U, Sabir H
Frontiers in neurology 2020;11:540878
Frontiers in neurology 2020;11:540878
CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer via Inhibiting JAK-STAT Signaling Pathway.
Chen B, Song L, Nie X, Lin F, Yu Z, Kong W, Qi X, Wang W
Frontiers in oncology 2020;10:577229
Frontiers in oncology 2020;10:577229
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Western blot analysis of CXCL1 in Lane 1: Jurkat cell lysate, Lane 2: HEK293T cell lysate, Lane 3: mouse heart tissue lysate, Lane 4: rat brain tissue lysate. Sample was incubated with CXCL1 polyclonal antibody (Product # PA5-86508) using a 1:500 dilution.
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Western blot was performed using Anti-CXCL1 Polyclonal Antibody (Product # PA5-86508) and a 9 kDa band corresponding to soluble cleaved form of CXCL1 was observed across cell lines tested. Conditioned media (20 µg lysate) of Caki-1, positive model (Lane 1) and HT-29, negative model (Lane 2) were electrophoresed using NuPAGE™ 12% Bis-Tris Protein Gel (Product # NP0341BOX). Resolved proteins were then transferred onto a nitrocellulose membrane (Product # IB23001) by iBlot® 2 Dry Blotting System (Product # IB21001). The blot was probed with the primary antibody (1:1000 dilution) and detected by chemiluminescence with Goat anti-Rabbit IgG (H+L) Superclonal™ Recombinant Secondary Antibody, HRP (Product # A27036,1:20,000 dilution) using the iBright FL 1000 (Product # A32752). Chemiluminescent detection was performed using SuperSignal™ West Atto Ultimate Sensitivity Substrate (Product # A38556).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunofluorescence analysis of Growth-regulated alpha protein was performed using 70% confluent log phase A-375 cells treated with 10 ng/mL TNF alpha for 24 hours and untreated A-375 cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 15 minutes, and blocked with 2% BSA for 1 hour at room temperature. The cells were labeled with CXCL1 Polyclonal Antibody (Product # PA5-86508) at 1:100 dilution in 0.1% BSA, incubated at 4°C overnight and then labeled with Donkey anti-Rabbit IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Alexa Fluor Plus 488 (Product # A32790), (1:2000 dilution), for 45 minutes at room temperature (Panel a: Green) in A-375 treated cells. Nuclei (Panel b:Blue) were stained with ProLong™ Diamond Antifade Mountant with DAPI (Product # P36962). F-actin (Panel c: Red) was stained with Rhodamine Phalloidin (Product # R415, 1:300). Panel d represents the merged image showing cytoplasmic localization in TNF alpha treated A-375 cells. Panel e represents untreated A-375 cells that show no expression of CXCL1. Panel f represents control cells with no primary antibody to assess background. The images were captured at 60X magnification.
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Knockdown of CXCL1 was achieved by transfecting A-375 cells with CXCL1 specific siRNA (Silencer® select Product # s6215 and s6216) followed by treatment with 10 ng/mL TNF alpha for 24 hours. Immunofluorescence analysis was performed on untransfected A-375 cells treated with TNF alpha (panel a-d), transfected with non-specific scrambled siRNA followed by TNF alpha treatment (panels e-h) and transfected with CXCL1 specific siRNA and TNF alpha treatment (panel i-l). Cells were fixed, permeabilized, and labelled with CXCL1 Rabbit Polyclonal Antibody (Product # PA5-86508), (1:100 dilution) followed by Goat anti-Rabbit IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Alexa Fluor Plus 488 (Product # A32731, 1:2000 dilution). Nuclei (blue) were stained with ProLong™ Diamond Antifade Mountant with DAPI (Product # P36962), and Rhodamine Phalloidin (Product # R415, 1:300) was used for cytoskeletal F-actin (Red) staining. Reduction of specific signal was observed upon siRNA mediated knockdown (panel i, l) confirming specificity of the antibody to CXCL1 (Green). The Images were captured at 60X magnification.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemical analysis of CXCL1 in paraffin-embedded human tonsil carcinoma tissue. Sample was incubated with polyclonal CXCL1 antibody (Product # PA5-86508) using a 1:50 dilution.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 6 The keratinocyte-target lipid-polymer nanohybrids suppress IMQ-induced cytokine and chemokine expression, as well as neutrophil infiltration in psoriasis-like skin. IHC analysis represents (A) IL-17, (B) CXCL1, (C) CXCL2, (D) Ki67 + , (E) Ly6G, and (F) MPO in psoriasis-like skin. Scale bars, 100 um.
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 7 CXCL1 promotes CRC proliferation in vivo via JAK-STAT signaling pathway. SW480 cells transfected with oe-NC, oe-CXCL1 and oe-CXCL1+AG490 were subcutaneously grafted into nude mice, respectively. (A) Tumor size and tumor weight after 4 weeks, (B) tumor volume in the first 4 weeks, (C) immunohistochemistry showed the levels of CXCL1 and Ki67 in cells (* p < 0.05).
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 4 CXCL1 protein expression in different brain regions after inflammation-sensitized hypoxic-ischemic brain injury. Twenty-four hours after hypoxia-ischemia the expression of CXCL1 protein is not regulated in cortex (A) , hippocampus (HIP) (B) or thalamus (TH) (C) from animals of both genders (Sham n = 7, LPS n = 5, Veh/HI n = 9, LPS n = 8). A significant upregulation is determined in cortex of males after inflammation-sensitized hypoxic-ischemic brain injury (A) , whereas there was no gender specific upregulation in hippocampus (B) or thalamus (C) (Sham n = 4 males, LPS n = 4 males, Veh/HI n = 4 males, LPS n = 4 males). * p < 0.05, ** p < 0.01.