Collagen I Recombinant Mouse Monoclonal Antibody [46D10]

货号：

AWA00725

应用：

WB,IHC-P,IF-C

反应性：

Human,Mouse,Rat

来源：

Mouse

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:

Mouse

Reactivity:

Human, Mouse, Rat

Molecular Wt:

139 kDa

Clonality:

Monoclonal

Isotype:

IgG2a

Concentration:

1mg/ml

Other Names:

Alpha 1 type I collagen; COL1A1; Collagen alpha 1(I) chain; Collagen type I alpha 1; EDSC; OI1; OI2; OI3; OI4; type I proalpha 1

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 1:1000-1:2000
IHC-P 1:100-1:1000
IF-C 1:100-1:800

Immunogen
Information

Gene Name:

COL1A1

Protein Name:

Collagen alpha-1(I) chain

Gene ID:

1277 (Human)
12842 (Mouse)
29393 (Rat)

SwissPro:

P02452 (Human)
P11087 (Mouse)
P02454 (Rat)

Immunogen
Information

Subcellular Location:

Secreted, extracellular space, extracellular matrix.

Immunogen:

Synthesized peptide derived from human Collagen I. AA range: 1200-1464.

Specificity:

Collagen I Monoclonal Antibody detects endogenous levels of Collagen I protein.

Product images
	Fig : Western blot analysis of Collagen I 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 (AWA00725, 1/1000) was used in TBST at room temperature for 2 hours. Goat Anti-Mouse IgG - HRP Secondary Antibody (AWS0001) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: SK-N-SH cell Lane 2: SAOS-2 cell Lane 3: Human colonic Lane 4: Human colon cancer Predicted molecular weight:139 kDa Observed molecular weight:139 kDa/~200 kDa Exposure time:15s

	Fig: Immunocytochemistry analysis of U2OS cells labeling COL1A1 with mouse anti-COL1A1 antibody (AWA00725) at 1/100 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 mouse anti-COL1A1 antibody (AWA00725) at 1/100 dilution in 2% negative goat serum overnight at 4 ℃. Goat Anti-mouse IgG H&L (iFluor™ 488, AWS0003) 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: Immunocytochemistry analysis of PANC-1 cells labeling COL1A1 with mouse anti-COL1A1 antibody (AWA00725) at 1/250 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 mouse anti-COL1A1 antibody (AWA00725) at 1/250 dilution in 2% negative goat serum overnight at 4 ℃. Goat Anti-mouse IgG H&L (iFluor™ 488, AWS0003) 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 : Immunohistochemical analysis of paraffin-embedded Rat-breast tissue with Mouse anti-COL1A1 (AWA00725) 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 (AWA00725) 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 Mouse-kidney tissue with Mouse anti-Collagen I antibody (AWA00725) at 1/500 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 (AWA00725) at 1/500 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.

引用文献 (1)

Journal of Orthopaedic Surgery and Research IF:2.8

Silencing p75NTR regulates osteogenic differentiation and angiogenesis of BMSCs to enhance bone healing in fractured rats

Background Fractures heal through a process that involves angiogenesis and osteogenesis but may also lead to non-union or delayed healing. Bone marrow mesenchymal stem cells (BMSCs) have been reported to play a pivotal role in bone formation and vascular regeneration and the p75 neurotrophin receptor (p75NTR) as being an important regulator of osteogenesis. Herein, we aim to determine the potential mediation of BMSCs by p75NTR in bone healing. Methods Rat BMSCs were identified by flow cytometry (FCM) to detect cell cycle and surface markers. Then transfection of si/oe-p75NTR was performed in BMSCs, followed by Alizarin red staining to detect osteogenic differentiation of cells, immunofluorescence double staining was performed to detect the expression of p75NTR and sortilin, co-immunoprecipitation (CO-IP) was conducted to analyze the interaction between p75NTR and sortilin, and EdU staining and cell scratch assay to assess the proliferation and migration of human umbilical vein endothelial cells (HUVECs). The expression of HIF-1α, VEGF, and apoptosis-related proteins were also detected. In addition, a rat fracture healing model was constructed, and BMSCs-si-p75NTR were injected, following which the fracture condition was observed using micro-CT imaging, and the expression of platelet/endothelial cell adhesion molecule-1 (CD31) was assessed. Results The results showed that BMSCs were successfully isolated, p75NTR inhibited apoptosis and the osteogenic differentiation of BMSCs, while si-p75NTR led to a decrease in sortilin expression in BMSCs, increased proliferation and migration in HUVECs, and upregulation of HIF-1α and VEGF expression. In addition, an interaction was observed between p75NTR and sortilin. The knockdown of p75NTR was found to reduce the severity of fracture in rats and increase the expression of CD31 and osteogenesis-related proteins. Conclusion Silencing p75NTR effectively modulates BMSCs to promote osteogenic differentiation and angiogenesis, offering a novel perspective for improving fracture healing.

pubTime 2024-03-20

Application

Specie

Rat

Dilution

1:2000