产品: ICAM1 抗体
货号: DF7413
描述: Rabbit polyclonal antibody to ICAM1
反应: Human
分子量: 57kDa; 58kD(Calculated).
蛋白号: P05362
RRID: AB_2839351


   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货



WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

ICAM1 Antibody detects endogenous levels of total ICAM1.
引用格式: Affinity Biosciences Cat# DF7413, RRID:AB_2839351.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
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.


Antigen identified by monoclonal antibody BB2; BB 2; BB2; CD 54; CD_antigen=CD54; CD54; Cell surface glycoprotein P3.58; Human rhinovirus receptor; ICAM 1; ICAM-1; ICAM1; ICAM1_HUMAN; intercellular adhesion molecule 1 (CD54), human rhinovirus receptor; Intercellular adhesion molecule 1; Major group rhinovirus receptor; MALA 2; MALA2; MyD 10; MyD10; P3.58; Surface antigen of activated B cells, BB2;


This gene encodes a cell surface glycoprotein which is typically expressed on endothelial cells and cells of the immune system. It binds to integrins of type CD11a / CD18, or CD11b / CD18 and is also exploited by Rhinovirus as a receptor.

翻译修饰 - P05362 作为底物

Site PTM Type Enzyme
S43 Phosphorylation
T62 O-Glycosylation
T62 Phosphorylation
N130 N-Glycosylation
N145 N-Glycosylation
N183 N-Glycosylation
N202 N-Glycosylation
Y207 Phosphorylation
T211 Phosphorylation
T217 Phosphorylation
S223 Phosphorylation
N267 N-Glycosylation
S275 Phosphorylation
N296 N-Glycosylation
S323 Phosphorylation
K359 Ubiquitination
N385 N-Glycosylation
Y501 Phosphorylation
Y512 Phosphorylation
K519 Ubiquitination
T521 Phosphorylation
K524 Ubiquitination
T527 Phosphorylation
T530 Phosphorylation



ICAM proteins are ligands for the leukocyte adhesion protein LFA-1 (integrin alpha-L/beta-2). During leukocyte trans-endothelial migration, ICAM1 engagement promotes the assembly of endothelial apical cups through ARHGEF26/SGEF and RHOG activation.

(Microbial infection) Acts as a receptor for major receptor group rhinovirus A-B capsid proteins.

(Microbial infection) Acts as a receptor for Coxsackievirus A21 capsid proteins.

(Microbial infection) Upon Kaposi's sarcoma-associated herpesvirus/HHV-8 infection, is degraded by viral E3 ubiquitin ligase MIR2, presumably to prevent lysis of infected cells by cytotoxic T-lymphocytes and NK cell.


Monoubiquitinated, which is promoted by MARCH9 and leads to endocytosis.


Membrane>Single-pass type I membrane protein.

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

Homodimer (Probable). Interacts with MUC1 and promotes cell aggregation in epithelial cells. Interacts with ARHGEF26/SGEF. Interacts (on T cell side) with CD81, CD247 and CD9 at immunological synapses between antigen-presenting cells and T cells.

(Microbial infection) Interacts with major receptor group rhinovirus A-B capsid proteins.

(Microbial infection) Interacts with Coxsackievirus A21 capsid proteins.


Belongs to the immunoglobulin superfamily. ICAM family.


· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cell adhesion molecules (CAMs).   (View pathway)

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

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Bacterial > Staphylococcus aureus infection.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Human Diseases > Cardiovascular diseases > Viral myocarditis.

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

· Organismal Systems > Immune system > Leukocyte transendothelial migration.   (View pathway)


1). A novel UV-curable extravascular stent to prevent restenosis of venous grafts. Composites Part B: Engineering [IF=13.1]

2). Zhao M et al. HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury. CELLULAR & MOLECULAR BIOLOGY LETTERS 2021 Sep 3;26(1):40. (PubMed: 34479471) [IF=8.3]

3). Smith AO et al. Novel Strategy for Isolation of Mice Bone Marrow–Derived Endothelial Cells (BMECs). Stem Cell Research & Therapy 2021 May 3;12(1):267. (PubMed: 33941266) [IF=7.5]

4). Yang F et al. Karyopherin α 2 promotes proliferation, migration and invasion through activating NF-κB/p65 signaling pathways in melanoma cells. LIFE SCIENCES 2020 Mar 31:117611 (PubMed: 32243925) [IF=6.1]

Application: WB    Species: Mice    Sample: melanoma cells

Fig. 4. KPNA2 activated NF-κB/p65 signaling pathway in melanoma cells. The expression of NF-κB p65, COX-2, ICAM-1, iNOS, MCP1, and p65 (nucleus) was analyzed by western blot in the KPNA2-overexpressing (A, B) or KPNA2-silenced cells (F, G). The nuclear translocation of p65 (nucleus) was detected by immunofluorescence assay in the KPNA2-overexpressing (C, D) or KPNA2-silenced cells (H, I). The NF-κB binding activity was analyzed by EMSA in the KPNA2- overexpressing (E) or KPNA2-silenced cells (J). Parental, blank control group; NC, negative control group; OV-KPNA2, KPNA2 overexpressed group; siRNA1-KPNA2, KPNA2-1 silencing group; siRNA2-KPNA2, KPNA2-2 silencing group. The results were obtained in three independent experiments. Mean values were compared by One-way ANOVA. (**p < 0.01, ***p < 0.001, ****p < 0.001).

5). Chen X et al. Galectin-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation. JOURNAL OF CELLULAR PHYSIOLOGY 2018 Dec 10 (PubMed: 30536538) [IF=5.6]

Application: WB    Species: human    Sample: HUVECs cells

FIGURE 6| Gal‐3 induced expression of inflammatory factors promoted HUVECs injury via integrin β1‐RhoA‐JNK pathway. HUVECs,exposing to the ox‐LDL alone or in combination with Gal‐3 were further treated with integrin β1‐siRNA or JNK inhibitor (SP600125). The total and phosphorylated expression of p65,IKKα and IKKβ after the above treatment was examined by WB and demonstrated by histogram. (a and b).The levels of inflammatory cytokines and chemokines were then measured by ELISA. (c and d) The expression of adhesion molecules (ICAM‐1 and VCAM‐1) was detected by WB (e). *p < 0.05, **p < 0.01

6). Ming-hao Ge et al. Zinc attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury by activating Nrf2/GPX4 defense pathway. CNS Neuroscience & Therapeutics 2021 May 5. (PubMed: 33951302) [IF=5.5]

Application: WB    Species: Mouse    Sample: Spinal cord

FIGURE 7 Zinc can reduce the inflammation of damaged parts by inhibiting ferroptosis. (A) The expressions of TNF-α, IL-6, IL-1β, and ICAM-1 were evaluated by Western blotting at 3 days post-SCI in each group (n = 6). (B) Quantification of TNF-α, IL-6, IL-1β, and ICAM-1 expressions (n = 6, all the data are expressed as means ± SD, two-way ANOVA followed by Tukey's post hoc test was applied). (C–F) Immunofluorescence staining was used to detect the level of TNF-α, IL-6, IL-1β, and ICAM-1 from each group (n = 6, scale bar = 50 µm). (G) Statistical analysis of immunofluorescence staining for positive expression of TNF-α, IL-6, IL-1β, and ICAM-1 in nerve cells from each group (n = 6, all the data are expressed as means ± SD, two-way ANOVA followed by Tukey's post hoc test was applied). * means p < 0.05; **means p < 0.01; and *** means p < 0.001

7). Liang PL et al. Guang Chen Pi (the pericarp of Citrus reticulata Blanco's cultivars 'Chachi') inhibits macrophage-derived foam cell formation. JOURNAL OF ETHNOPHARMACOLOGY 2022 Jul 15;293:115328. (PubMed: 35489660) [IF=5.4]

8). Huang S et al. Nepeta angustifolia attenuates responses to vascular inflammation in high glucose-induced human umbilical vein endothelial cells through heme oxygenase-1 induction. JOURNAL OF ETHNOPHARMACOLOGY 2019 Mar 1;231:187-196 (PubMed: 30419276) [IF=5.4]

9). Li K et al. Wenyang Huazhuo Tongluo formula alleviates pulmonary vascular injury and downregulates HIF-1α in bleomycin-induced systemic sclerosis mouse model. BMC Complementary Medicine and Therapies 2022 Jun 22;22(1):167. (PubMed: 35733188) [IF=3.9]

Application: IF/ICC    Species: Mouse    Sample:

Fig. 5Wenyang Huazhuo Tongluo Formula and KC7F2 can significantly inhibit the expression of vWF, SELE, ICAM-1 and VCAM-1 in bleomycin-induced SSc mouse model. The effect of Wenyang Huazhuo Tongluo Formula and KC7F2 on the expression of vWF (A), SELE (B), ICAM-1 (C) and VCAM-1 (D) was observed by immunofluorescence staining. compared with the PBS group, bleomycin can significantly upregulate the expression levels of vWF, SELE, ICAM-1 and VCAM-1 in endothelial cells, while Wenyang Huazhuo Tongluo Formula and KC7F2 can significantly reverse the bleomycin-induced upregulation of vWF, SELE, ICAM-1 and VCAM-1. The mean values ± SD was shown for each bar. * (P < 0.05) or ** (P < 0.01) or *** (P < 0.001) represents significance, ns represents no significance. Original magnification: × 20. BLM: Bleomycin, WYHZTL: Wenyang Huazhuo Tongluo formula

10). Wang et al. Therapeutic effect and mechanism of 4‑phenyl butyric acid on renal ischemia‑reperfusion injury in mice. Experimental and Therapeutic Medicine 2022 Feb;23(2):144. (PubMed: 35069825) [IF=2.7]



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