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Invitrogen

VCAM-1 (CD106) Recombinant Rabbit Monoclonal Antibody (SA05-04)

11个已发表图片

7 篇参考文献

查看其他65个VCAM-1 (CD106)抗体

货号 MA5-31965

飞享价 CNY 2,999.00 4,917.00

活动截止日期 31-Mar-2025

100 µL

下单后预计有货时间 01-Apr-2025

批量或定制请求

Application

VCAM-1 (CD106) Antibody in Immunocytochemistry (ICC/IF)

图: 1 / 19

VCAM-1 (CD106) Antibody (MA5-31965) in ICC/IF

Immunofluorescence analysis of Vascular cell adhesion protein 1 was performed using 70% confluent log phase HUVEC 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 45 minutes at room temperature. The cells were labeled with VCAM-1 (CD106) Recombinant Rabbit Monoclonal Antibody (SA05-04) (Product # MA5-31965)... View More

VCAM-1 (CD106) Antibody in Immunocytochemistry (ICC/IF)

VCAM-1 (CD106) Antibody in Immunocytochemistry (ICC/IF)

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P))

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P))

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P))

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Immunohistochemistry (IHC)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody in Western Blot (WB)

VCAM-1 (CD106) Antibody

Product Image Gallery

VCAM-1 (CD106) Antibody in Immunocytochemistry (ICC/IF) — Immunofluorescence analysis of Vascular cell adhesion protein 1 was performed using 70% confluent log phase HUVEC 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 45 minutes at room temperature. The cells were labeled with VCAM-1 (CD106) Recombinant Rabbit Monoclonal Antibody (SA05-04) (Product # MA5-31965) at 1:100 in 0.1% BSA, incubated at 4 degree celsius 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). 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. Panel e represents control cells with no primary antibody to assess background. The images were captured at 60X magnification.

VCAM-1 (CD106) Antibody in Immunocytochemistry (ICC/IF) — Immunocytochemical analysis of VCAM-1 (CD106) in HUVEC cells using a VCAM-1 (CD106) Monoclonal antibody (Product # MA5-31965) as seen in green. The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P)) — Immunohistochemical analysis of VCAM-1 (CD106) of paraffin-embedded Mouse spleen tissue using a VCAM-1-CD106 Monoclonal antibody (Product #MA5-31965). Counter stained with hematoxylin.

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P)) — Immunohistochemical analysis of VCAM-1 (CD106) of paraffin-embedded Human spleen tissue using a VCAM-1-CD106 Monoclonal antibody (Product #MA5-31965). Counter stained with hematoxylin.

VCAM-1 (CD106) Antibody in Immunohistochemistry (Paraffin) (IHC (P)) — Immunohistochemical analysis of VCAM-1 (CD106) of paraffin-embedded Human tonsil tissue using a VCAM-1-CD106 Monoclonal antibody (Product #MA5-31965). Counter stained with hematoxylin.

VCAM-1 (CD106) Antibody in Western Blot (WB) — Western blot was performed using Anti-VCAM-1 (CD106) Recombinant Rabbit Monoclonal Antibody (SA05-04) (Product # MA5-31965) and an 80 kDa band corresponding to Vascular cell adhesion protein 1 was induced in HUVEC cells on treatment and also in tissues tested. An additional band around 35 kDa corresponding to the lower isoform was observed on the TNF alpha treatment. Membrane enriched extracts (30 µg lysate) of HUVEC (Lane 1), HUVEC treated with TNF alpha (10 ng/mL, for 6hrs)(Lane 2), HUVEC treated with Lipopolysaccharide (100 ng/mL, 4hrs) (Lane 3), Mouse Spleen (Lane 4) and Rat Spleen (Lane 5) were electrophoresed using NuPAGE™ 4-12% Bis-Tris Protein Gel (Product # NP0322BOX). 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 (Heavy Chain) Superclonal™ Recombinant Secondary Antibody, HRP (Product # A27036,1:4000 dilution) using the iBright FL 1000 (Product # A32752). Chemiluminescentdetection was performed using Novex® ECL Chemiluminescent Substrate Reagent Kit (Product # WP20005).

VCAM-1 (CD106) Antibody in Western Blot (WB) — Western blot analysis of VCAM-1 (CD106) in different lysates using a Monoclonal antibody (Product #MA5-31965) at a dilution of 1:1,000. Positive control: Lane 1: NIH/3T3.

VCAM-1 (CD106) Antibody in Immunohistochemistry (IHC) — Figure 3 C3 deficiency or CR2-Crry significantly inhibits the activation of neutrophils and decreases the expression of VCAM-1 and Mac-1 in mice with CLI. Wild-type and C3 deficient mice were subjected to BDL or sham operations. WT-BDL mice were injected i.p. with PBS or CR2-Crry and sacrificed 3 days later. Formalin-fixed, paraffin-embedded liver sections were stained for specific esterase or immunostained for MPO, 3-chlorotyrosine and VCAM-1. Anticoagulated blood was subjected to flow cytometry for Mac-1 detection. (A) Specific esterase staining for neutrophils and immunohistochemical staining for VCAM-1 in liver parenchyma. (B) Expression of Mac-1 on neutrophils. (C) Assessment of neutrophils in the liver portal area. (D) Immunohistochemical staining for MPO and 3-chlorotyrosine. Scale bars for all, 100 mum; n = 5-6 per group. Black arrows, positive staining in the liver parenchyma; red arrows, positive staining in the portal area. Results are expressed as mean +- SD. *p < 0.05, **p < 0.01; NS, not significant.

VCAM-1 (CD106) Antibody in Western Blot (WB) — Fig. 2 EGF-induced alteration of inflammatory and vasculogenic signals in M1 macrophages. ( A ) Real-time RT-PCR analysis for IL6, IL1B, TNFA, IL10, CD68, CD86, VEGFA, and VEGFC genes with and without EGF treatment in M1 macrophages ( N = 4 to 7). ( B ) The representative Western blot image for EGF precursor, VCAM-1, IL-1beta, VEGF-A, and IL-10 protein in M1 macrophages with and without EGF treatment. The small gaps indicate skipped lanes from the same membrane. Full-length gels before cropping are noted in Fig. S4 . ( C ) The result of ELISA for IL-6 levels in M0, M1, and M1 with EGF treatment ( N = 7). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, ns: not significant. EGF, epidermal growth factor; IL, interleukin; VEGF, vascular endothelial growth factor; VCAM-1, vascular cell adhesion molecule 1. Fig. 2

VCAM-1 (CD106) Antibody in Western Blot (WB) — Figure 3 miR-143-3p impaired autophagic degradation of CAMs through targeting ATP6V1A. A) PCR assay of the mRNA level of VCAM-1, ICAM-1, and PECAM-1 in hCMEC/D3 cells transfected with miR-143-3p minics or miR-nc ( n = 6 per group, Student's t-test). B) WB analysis of the levels of VCAM-1, ICAM-1, and PECAM-1 in human hCMEC/D3 cells after the treatment of the lysosomal proteases inhibitor bafilomycin A1 ( n = 6 per group, Student's t-test). C,D) Western blot analysis of the levels of LC3B-II and SQSTM1 in rapamycin-treated hCMEC/D3 cells transfected with miR-143-3p minics or miR-nc ( n = 6 per group, one-way ANOVA). E) Representative images and quantification of autophagic flux in rapamycin-treated hCMEC/D3 cells transfected with miR-143-3p minics or miR-NC ( n = 3 per group, one-way ANOVA). hCMEC/D3 cells were infected with GFP-mRFP-LC3 adenovirus. The intensity of red puncta and yellow puncta were determined. Scale bar: 10 um. F) Venn diagram showing the targeted genes of miR-143-3p predicted by TargetScan, miRanda, miRDB, and miRWalk databases. G) Overlap the predicted genes with the top 500 lysosomal function-related genes in GeneCards Database. Thus, two candidate genes (ATP6V1A, RNF152) that both were predicted to be the target of miR-143-3p and are correlated with lysosomal function were screened out. H) The predicted binding sites of miR-143-3p in ATP6V1A-3' UTR among different species. I) The detection of Lysosomal pH in hCMEC/D3 cells treated with miR-nc or miR-143-3

VCAM-1 (CD106) Antibody in Western Blot (WB) — Activated astrocytes transferred miR-143-3p into BMECs through EVs and promoted endothelial CAMs expression after ICH. A) qRT-PCR analysis of the level of EVs-miR-143-3p in the perihematomal brain tissues of mice at 24 h post-ICH, compared to that in sham group mice ( n = 6 per group; Student's t-test). B) The level of miR-143-3p in EVs derived from the culture supernatants of human SH-SY5Y (neuron), NHA (astrocyte), or HMC3 (microglia) cell lines with or without OxyHb treatment ( n = 6 per group, Student's t-test). C) The level of miR-143-3p in EVs derived from the culture supernatants of primary neurons, astrocytes, and microglia with or without OxyHb treatment ( n = 6 per group, Student's t-test). D) Representative immunofluorescence images of mouse brain sections after stereotactically injecting AAV-SMPD3-shRNA that contains a GFAP-specific promoter for 3 weeks. Scale bars, 50 um. E) qRT-PCR analysis of the level of EVs-miR-143-3p in the perihematomal brain tissues of ICH mice with or without astrocytes-specific knockdown of SMPD3 ( n = 6 per group, Student's t-test). F) Confocal imaging showing the absorption of PKH26-labeled EVs that derived from NHAs cells in hCMEC/D3 cells. hCMEC/D3, human brain microvascular endothelial cell line. Scale bar: 100 um. G) The level of miR-143-3p in hCMEC/D3 cells was quantified after the incubation of EVs derived from NHAs ( n = 6 per group, Student's t-test). H) qRT-PCR analysis of the level of miR-143-3p in isolated BMECs from ICH mic

VCAM-1 (CD106) Antibody in Western Blot (WB) — Endothelial-specific ATP6V1A knockout increased CAMs expression and neutrophil infiltration after ICH in mice. A) Establishment of endothelial-specific ATP6V1A knockout mice. B) Western blot assay of the expression of CAMs including VCAM-1, PECAM-1, and ICAM-1 at 24 h post-ICH in ATP6V1A fl/fl and ATP6V1A CKO mice ( n = 6 per group, one-way ANOVA). C) Representative gating strategy for flow cytometric analysis of immune cells in the brain at 24 h post-ICH in ATP6V1A fl/fl and ATP6V1A CKO mice. D-G) Cell surface antibodies were used to identify different cell types including D) Ly6G + neutrophils, E) Ly6G - Ly6C macrophage/monocytes, F) CD3e+ T cells, G) NK1.1+ NK cells ( n = 6 per group, one-way ANOVA). H) The expression of IL-1beta, IL-6, and TNF-a in the brain at 24 h after ICH in ATP6V1A fl/fl and ATP6V1A CKO mice was analyzed by ELISA ( n = 6 mice per group, one-way ANOVA). I) MRI images and quantification of hematoma at 24 h after ICH in ATP6V1A fl/fl and ATP6V1A CKO mice. Red lines delineate the lesion area. ( n = 6 per group, one-way ANOVA). J) Brain water content at 24 h after ICH in ATP6V1A fl/fl and ATP6V1A CKO mice ( n = 6 per group, one-way ANOVA). K) Representative images and statistical analysis of TUNEL-positive cells in mice brain sections. Data are represented as the percentage of TUNEL-positive cells ( n = 6 per group, Student's t-test). Scale bar: 50 um. Data are presented as means +- SD. * p < 0.05, ** p < 0.01, *** p < 0.0

VCAM-1 (CD106) Antibody in Western Blot (WB) — The detrimental role of EVs-miR-143-3p in TBI and the therapeutic effects of Vt-miR-143-3pi-EVs treatment. A) Relative plasma EVs-miR-143-3p level on the 1st day in TBI patients with poor (GOS 1-3) outcomes versus good (GOS 4-5) outcomes 6 months later. n = 67 in good outcome group and n = 46 in poor outcome group. GOS:Glasgow Outcome Scale. B) ROC curve for individual serum EVs-miR-143-3p level on day 1 to separate poor (GOS 1-3) outcomes versus good (GOS 4-5) outcomes 6 months later. C,D) Pearson analyses of the correlations of EVs-miR-143-3p with the serum levels of s-VCAM-1, and s-ICAM-1 within 24 h after TBI onset in patients ( n = 113). E) Western blot assay of the effects of Vt-miR-143-3pi-EVs on the expression of CAMs including ICAM-1, VCAM-1, and PECAM-1 in BMECs at 24 h post-TBI in each group mice ( n = 6 per group, one-way ANOVA). F) Flow cytometric analysis of the effects of Vt-miR-143-3pi-EVs on the infiltration of Ly6G+ neutrophils in the brain at day 1 post-TBI in mice ( n = 6 per group, one-way ANOVA). G) Representative images and statistical analysis of TUNEL-positive cells in mice brain sections at 24 h post-TBI in each group mice ( n = 6 per group, Student's t-test). Data are represented as the percentage of TUNEL-positive cells. Scale bar: 50 um. H) Measurement of brain water content at 24 h after TBI in each group mice ( n = 6 per group, one-way ANOVA). I-N) Several behavioral tests including foot fault test, adhesive test, and Morris water maze (MWM) tes

VCAM-1 (CD106) Antibody in Western Blot (WB) — Therapeutic effects of VCAM-1-targeting, miR-143-3p inhibitor-encapsulated EVs on ICH in mice. A) Experimental schematic. B,C) Western blot assay of the effects of Vt-miR-143-3pi-Evs on the expression of CAMs including ICAM-1, VCAM-1, and PECAM-1 in isolated BMECs at 24 h post-ICH in mice ( n = 6 per group, one-way ANOVA). D,E) Flow cytometric analysis of the effects of Vt-miR-143-3pi-Evs on the infiltration of Ly6G+ neutrophils in the brain at day 1 post-ICH in mice ( n = 6 per group, one-way ANOVA). F) Representative images and statistical analysis of TUNEL-positive cells in mice brain sections at 24 h post-ICH in each group mice ( n = 6 per group, Student's t-test). Data are represented as the percentage of TUNEL-positive cells. Scale bar: 50 um. G) Measurement of brain water content at 24 h after ICH in each group mice ( n = 6 per group, one-way ANOVA). H-J) Several behavioral tests including a foot fault test, rotarod test, and adhesive test were conducted to determine the neurological function of mice ( n = 12 per group, two-way ANOVA). Data are presented as means +- SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

VCAM-1 (CD106) Antibody in Western Blot (WB) — Expression of adhesive molecules and occludin in HUVEC cells treated with LPS, IS, and PA. ( A ) Western-bott results; ( B - D ) The band signal strength of VCAM-1, E-selectin, and occludin. The band signal strength of controls (untreated and vehicle-treated cells) was set to 1, and the values were normalized to beta-actin levels. Statistically significant differences vs control *p < 0.05; vs VC # p < 0.05; with vs without PA & p < 0.05.

VCAM-1 (CD106) Antibody in Western Blot (WB) — Figure 6 lncRNA XIST alleviates a vascular endothelial inflammation response and regulates migration and tube formation of bEnd3 cells under OGD/R conditions by targeting miR-92a (A) Representative images of western blot for the expression of Itgalpha5, KLF4, E-selectin, VCAM-1, ICAM-1, p-NF-kappaB, Claudin-5, and ZO-1 in bEnd3 cells co-transfected with the si-Ctl or si-XIST and/or miR-92a inhibitor (miR-92a-I) at 24 h restoration from OGD. (B-I) Bar graphs show the quantitative analyses of western blots as ratios of Itgalpha5/beta-actin (B), KLF4/beta-actin (C), E-selectin/beta-actin (D), VCAM-1/beta-actin (E), ICAM-1/beta-actin (F), p-NF-kappaB/total NF-kappaB (G), Claudin-5/beta-actin (H), and ZO-1/beta-actin (I) (n = 4 per experimental group). Note that the expressions of Itgalpha5, KLF4, and TJPs (Claudin-5 and ZO-1) in the si-XIST + NC inhibitor (NC-I)-treated bEnd3 cells markedly decreased, but the expressions of three CAMs including E-selectin, VCAM-1, and ICAM-1 and the p-NF-kappaB were significantly elevated relative to the si-Ctl + NC-I-treated group at 24 h restoration from OGD. However, these effects were significantly rescued by inhibiting the levels of miR-92a in the bEnd3 cells. *p < 0.05, **p < 0.01, and ***p < 0.001. (J) Representative images of cell migration and capillary tube formation of bEnd3 cells transfected with si-Ctl or si-XIST and/or miR-92a-I after OGD/R treatment. Scale bar, 400 mum for migration; 500 mum for tube formation. (K and L) Quantifica

VCAM-1 (CD106) Antibody in Western Blot (WB) — Figure 5 Overexpression of Itgalpha5 or KLF4 reverses the effect of lncRNA XIST on the migration and tube formation and the expression of three CAMs, p-NF-kappaB, and TJPs of bEnd3 cells under OGD/R conditions (A) Representative images of western blot for the expression of Itgalpha5 in bEnd3 cells co-transfected with si-XIST and Itgalpha5 overexpression plasmid at 24 h restoration from OGD. (B) Bar graphs show the quantitative analyses of western blots as ratios of Itgalpha5/beta-actin (n = 4 per experimental group). (C) Representative images of cell migration and capillary tube formation of bEnd3 cells co-transfected with si-XIST and Itgalpha5 overexpression plasmid after OGD/R treatment. Scale bar, 400 mum for migration; 500 mum for tube formation. (D and E) Quantification of cell migration (D) and tube formation (E) of bEnd3 cells (n = 4 per experimental group). (F) Representative images of western blot for the expression of KLF4, three CAMs (E-selectin, VCAM-1, and ICAM-1), p-NF-kappaB, and TJPs (Claudin-5 and ZO-1) in bEnd3 cells co-transfected with si-XIST and KLF4 overexpression plasmid at 24 h restoration from OGD. (G-M) Bar graphs show the quantitative analyses of western blots as ratios of KLF4/beta-actin (G), E-selectin/beta-actin (H), VCAM-1/beta-actin (I), ICAM-1/beta-actin (J), p-NF-kappaB/total NF-kappaB (K), Claudin-5/beta-actin (L), and ZO-1/beta-actin (M) (n = 4 per experimental group). Note that bEnd3 cells co-transfected with si-XIST and Itgalpha5 displaye

VCAM-1 (CD106) Antibody in Western Blot (WB) — Figure 4 The influence of silencing of lncRNA XIST on the migration and tube formation and the expression of Itgalpha5, KLF4, three CAMs, phosphorylation of (p)-NF-kappaB, and TJPs of bEnd3 cells under OGD/R conditions (A) Representative images of western blot for the expression of Itgalpha5, KLF4, three CAMs (E-selectin, VCAM-1, and ICAM-1), p-NF-kappaB, and TJPs (Claudin-5 and ZO-1) in bEnd3 cells transfected with the negative control siRNA (si-Ctl) or siRNA-lncRNA XIST (si-XIST) at 24 h restoration from OGD. The NO-OGD/R cells served as a control. (B-I) Bar graphs show the quantitative analyses of western blots as ratios of Itgalpha5/beta-actin (B), KLF4/beta-actin (C), E-selectin/beta-actin (D), VCAM-1/beta-actin (E), ICAM-1/beta-actin (F), p-NF-kappaB/total NF-kappaB (G), Claudin-5/beta-actin (H), and ZO-1/beta-actin (I) (n = 4 per experimental group). Note that the expressions of Itgalpha5, KLF4, and TJPs (Claudin-5 and ZO-1) in the si-XIST-treated bEnd3 cells were markedly reduced, but the expressions of three CAMs including E-selectin, VCAM-1, and ICAM-1 and the p-NF-kappaB were significantly elevated relative to the si-Ctl-treated group at 24 h restoration from OGD. *p < 0.05, **p < 0.01, and ***p < 0.001. (J) Representative images of cell migration and capillary tube formation of bEnd3 cells transfected with si-Ctl or si-XIST after OGD/R treatment. Scale bar, 400 mum for migration; 500 mum for tube formation. (K) Quantification of cell migration of bEnd3 cells. The

VCAM-1 (CD106) Antibody — Altered expression of proteins upon cell treatment demonstrates antibody specificity. Western blot using VCAM-1 (CD106) Recombinant Rabbit Monoclonal Antibody (SA05-04)(Product # MA5-31965), shows an increase in VCAM-1 expression (80 and 35 kDa) in HUVEC cells on TNF alpha (10 ng/mL, 6hrs) and Lipopolysaccharide (100 ng/mL, 4hrs) treatment. {TM}

产品信息

MA5-31965

应用

建议稀释比

已发表文章

免疫印迹 (WB)

1:2000-1:5000

查看5篇已发表文章 5篇已发表文章

免疫组化 (IHC)

-

查看1篇已发表文章 1篇已发表文章

免疫组化（石蜡） (IHC (P))

1:200

-

免疫组化（冰冻） (IHC (F))

-

查看1篇已发表文章 1篇已发表文章

免疫细胞化学 (ICC/IF)

1:1000

-

产品规格

种属反应

Human, Mouse, Rat, Zebrafish

已发表种属

Mouse

宿主/亚型

Rabbit / IgG

Expression System

HEK293 cells

分类

Recombinant Monoclonal

类型

Antibody

克隆号

SA05-04

抗原

Synthetic peptide within Human VCAM1 aa 690-739

查看免疫原

偶联物

Unconjugated

形式

Liquid

浓度

1 mg/mL

纯化类型

Protein A

保存液

TBS, pH 7.4, with 40% Glycerol, 0.05% BSA

内含物

0.05% sodium azide

保存条件

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

运输条件

Ambient (domestic); Wet ice (international)

RRID

AB_2809259

产品详细信息

Recombinant rabbit monoclonal antibodies are produced using in vitro expression systems. The expression systems are developed by cloning in the specific antibody DNA sequences from immunoreactive rabbits. Then, individual clones are screened to select the best candidates for production. The advantages of using recombinant rabbit monoclonal antibodies include: better specificity and sensitivity, lot-to-lot consistency, animal origin-free formulations, and broader immunoreactivity to diverse targets due to larger rabbit immune repertoire.

靶标信息

VCAM-1 is a cell surface sialoglycoprotein expressed by cytokine activated endothelium. The protein has a number of functions including the regulation of leukocyte migration, leukocyte-endothelial cell adhesion and signal transduction and may play a role in a number of inflammatory diseases.

仅用于科研。不用于诊断过程。未经明确授权不得转售。

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生物信息学

蛋白别名: CD106; CD106 antigen; DKFZp779G2333; INCAM-100; INCAM100; MGC99561; sCD106; soluble CD106; soluble VCAM 1; sVCAM 1; V-CAM 1; Vascular cell adhesion protein 1; VCAM-1

基因别名: CD106; INCAM-100; Vcam-1; VCAM1; VCAM1B

UniProt ID: (Human) P19320, (Rat) P29534

Entrez Gene ID: (Human) 7412, (Rat) 25361, (Mouse) 22329

integrin binding primary amine oxidase activity cell adhesion molecule binding

参与通路

response to hypoxia acute inflammatory response chronic inflammatory response cell adhesion heterophilic cell-cell adhesion via plasma membrane cell adhesion molecules leukocyte cell-cell adhesion cell-matrix adhesion heart development aging response to nutrient amine metabolic process response to zinc ion response to ionizing radiation viral process membrane to membrane docking response to lipopolysaccharide response to nicotine cellular response to vascular endothelial growth factor stimulus positive regulation of T cell proliferation response to ethanol leukocyte tethering or rolling oxidation-reduction process cell chemotaxis embryonic placenta morphogenesis chorio-allantoic fusion cellular response to glucose stimulus cellular response to tumor necrosis factor B cell differentiation extracellular matrix organization calcium-mediated signaling using intracellular calcium source regulation of immune response interferon-gamma-mediated signaling pathway single organismal cell-cell adhesion visceral serous pericardium development