Gasdermin D(N terminal) Rabbit Polyclonal Antibody

货号：

AWA75002

应用：

WB,IHC-P,IF,FCM

反应性：

Human,Mouse,Rat,Pig

来源：

Rabbit

规格 价格 库存
20μL ¥620 1-3个工作日
50μL ¥1250 1-3个工作日
100μL ¥2200 1-3个工作日

产品概述

Product Details

Host Species:

Rabbit

Reactivity:

Human, Mouse, Rat, Pig

Molecular Wt:

Predicted MW: 53 kDa
Observed MW: 53, 35 kDa

Clonality:

Polyclonal

Isotype:

IgG

Concentration:

1.108mg/ml

Other Names:

Gasdermin-D; Gasdermin-D; gasderminD; Gasdermin domain-containing protein 1; gasdermin D; DF5L; DFNA5L; FKSG10; GSDMDC1; GSDMD; Gasdermin D(N terminal)

Formulation:

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Purification:

Affinity-chromatography

Storage:

Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20°C storage.

Applications

WB 1:1000-1:5000
IHC-P 1:100-1:1000
IF 1:100-1:800
FCM 1:50-1:200

Immunogen
Information

Gene Name:

GSDMD

Protein Name:

Gasdermin-D

Gene ID:

79792 (Human)
69146 (Mouse)

SwissPro:

P57764 (Human)
Q9D8T2 (Mouse)

Immunogen
Information

Subcellular Location:

Cytoplasm, cytosol. Inflammasome. Cell membrane. Secreted. Mitochondrion membrane.

Immunogen:

Synthetic peptide of human Gasdermin D. AA range: 56-70.

Specificity:

Gasdermin D(N terminal) Polyclonal Antibody detects endogenous levels of Gasdermin D(N terminal) protein.

Product images
	Fig: Immunocytochemistry analysis of PC-3 cells labeling Gasdermin D(N terminal) with Rabbit anti-Gasdermin D(N terminal) antibody (AWA75002) at 1/300 dilution(green). Cells were fixed in 4% paraformaldehyde for 10 minutes at 37 ℃, permeabilized with 0.03% Triton X-100 in PBS for 30 minutes, and then blocked with 5% BSA for 60 minutes at 37 ℃. Cells were then incubated with Rabbit anti-Gasdermin D(N terminal) antibody (AWA75002) at 1/300 dilution in 2% negative goat serum overnight at 4 ℃. Goat Anti-Rabbit IgG H&L (iFluor™488, AWS0005) was used as the secondary antibody at 1/200 dilution for 60 minutes at 37 ℃. Nuclear DNA was labelled in blue with DAPI(AWC0291).

	Fig : Western blot analysis of Gasdermin D(N terminal) on different lysates. Proteins were transferred to a NC membrane and blocked with 5% NF-Milk in TBST for 1 hour at room temperature. The primary antibody (AWA75002, 1/1000) was used in TBST at room temperature for 2 hours. Goat Anti-Rabbit IgG - HRP Secondary Antibody (AWS0002) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: PC12 cell Lane 2: SIHa cell Lane 3: CAL27 cell Lane 4: Rat stomach Lane 5: CAKI-1 cell Lane 6: THP-1 cell Lane 7: 3D4/21 cell Lane 8: A431 cell Lane 9: HT1080 cell Predicted molecular weight:53 kDa Observed molecular weight:53 kDa(GSDMD)；35KD(GSDMD N-Terminal)

	Fig : Immunohistochemical analysis of paraffin-embedded Rat-kidney tissue with Rabbit anti-Gasdermin D(N terminal) (AWA75002) at 1/200 dilution. The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H₂O₂ for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA75002) at 1/200 dilution for 1 hour at room temperature. The detection was performed using an HRP conjugated compact polymer system(ABIOWELL, AWI0629). DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX.

	Fig : Immunohistochemical analysis of paraffin-embedded Rat-lung tissue with Rabbit anti-Gasdermin D(N terminal) (AWA75002) at 1/200 dilution. The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H₂O₂ for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA75002) at 1/200 dilution for 1 hour at room temperature. The detection was performed using an HRP conjugated compact polymer system(ABIOWELL, AWI0629). DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX.

	Fig：Flow cytometric analysis of RAW264.7 cells labeling Gasdermin D(N terminal). Overlay histogram showing RAW264.7 cells stained with Gasdermin D(N terminal) (green line). The cells were fixed in 4% paraformaldehyde for 30 minutes at 37 ℃, permeabilized with 0.02% Triton X-100 in PBS for 30 minutes,and then stained with the primary antibody(AWA75002, 1µg/1x106 cells) for 30 min at 4°C. The secondary antibody used was an Alexa Fluor 488-conjugated Goat anti-Rabbit IgG Secondary antibody (AWS0005b) at 1/1000 dilution for 30 min at 4ºC. Unlabelled sample was used as a control (cells without incubation with primary antibody; red).

引用文献 (1)

Frontiers in Immunology IF:5.9

Integrative Mendelian randomization and experimental validation prioritize KLF4 in the gut microbiota–pyroptosis–barrier axis of ulcerative colitis

Background Ulcerative colitis (UC) arises from complex crosstalk between gut microbiota, epithelial barrier integrity, and inflammatory cell death, yet causal mediators along this axis remain poorly defined. We aimed to delineate microbiota–pyroptosis–UC pathways and functionally validate key effectors, with a focus on KLF4. Methods A multistage framework integrating genome-wide association studies of gut microbiota (MiBioGen), plasma proteomics (deCODE), and UC (UK Biobank) was constructed to perform two-sample Mendelian randomization (MR). Pyroptosis-related proteins were screened for causal associations with UC, followed by MR of UC-associated microbial taxa on these proteins and two-step mediation analysis. KLF4 was further evaluated using bulk and single-cell transcriptomic datasets, including virtual knockout network perturbation. Its clinical relevance was tested in two cohorts of UC patients receiving anti-TNF-α therapy. Finally, the KLF4 function was validated in a dextran sulfate sodium (DSS)-induced colitis model with systemic AAV9-mediated KLF4 overexpression. Results MR identified 35 pyroptosis-related plasma proteins and 23 microbial taxa with putative causal effects on UC. Mediation analysis highlighted MAPK11, PTEN, and KLF4 as dominant intermediates linking specific taxa to UC risk. KLF4 was consistently downregulated in UC, and low KLF4 expression was associated with enrichment of pro-inflammatory and immune-activation signatures. Higher mucosal KLF4 levels predicted response to anti-TNF-α therapy with moderate discriminatory performance. In DSS-induced colitis, KLF4 overexpression mitigated weight loss and disease activity, preserved colon length, improved histology, and reduced myeloperoxidase activity. KLF4 restored Claudin-1, Occludin, and Zo-1; suppressed Claudin-2; decreased intestinal permeability; limited gasdermin-D (GSDMD) cleavage; lowered IL-1β/IL-18 levels; and reshaped splenic leukocyte composition. Conclusions Our integrative genetic and experimental data position KLF4 as a central node in a gut microbiota–pyroptosis–barrier axis in UC, supporting KLF4 as a promising biomarker and therapeutic target for the precision management of UC.

pubTime 2026-03-16

Application

Specie

Mouse

Dilution