Product: ICAM1 Antibody
Catalog: DF7413
Description: Rabbit polyclonal antibody to ICAM1
Application: WB IHC IF/ICC
Reactivity: Human
Mol.Wt.: 57kDa; 58kD(Calculated).
Uniprot: P05362
RRID: AB_2839351

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 100ul $280 In stock
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Product Info

Source:
Rabbit
Application:
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.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human
Clonality:
Polyclonal
Specificity:
ICAM1 Antibody detects endogenous levels of total ICAM1.
RRID:
AB_2839351
Cite Format: Affinity Biosciences Cat# DF7413, RRID:AB_2839351.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
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.
Sequence:
MAPSSPRPALPALLVLLGALFPGPGNAQTSVSPSKVILPRGGSVLVTCSTSCDQPKLLGIETPLPKKELLLPGNNRKVYELSNVQEDSQPMCYSNCPDGQSTAKTFLTVYWTPERVELAPLPSWQPVGKNLTLRCQVEGGAPRANLTVVLLRGEKELKREPAVGEPAEVTTTVLVRRDHHGANFSCRTELDLRPQGLELFENTSAPYQLQTFVLPATPPQLVSPRVLEVDTQGTVVCSLDGLFPVSEAQVHLALGDQRLNPTVTYGNDSFSAKASVSVTAEDEGTQRLTCAVILGNQSQETLQTVTIYSFPAPNVILTKPEVSEGTEVTVKCEAHPRAKVTLNGVPAQPLGPRAQLLLKATPEDNGRSFSCSATLEVAGQLIHKNQTRELRVLYGPRLDERDCPGNWTWPENSQQTPMCQAWGNPLPELKCLKDGTFPLPIGESVTVTRDLEGTYLCRARSTQGEVTRKVTVNVLSPRYEIVIITVVAAAVIMGTAGLSTYLYNRQRKIKKYRLQQAQKGTPMKPNTQATPP

PTMs - P05362 As Substrate

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

Research Backgrounds

Function:

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.

PTMs:

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

Subcellular Location:

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
Subunit Structure:

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.

Family&Domains:

Belongs to the immunoglobulin superfamily. ICAM family.

Research Fields

· 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)

References

1). A novel UV-curable extravascular stent to prevent restenosis of venous grafts. Composites Part B: Engineering, 2021 [IF=13.1]

Application: WB    Species: Rat    Sample:

Fig. 6. A: PCNA immunofluorescence staining of venous graft vessels in rats. B, C: Western blot analysis of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. D: ICAM-1 immunofluorescence staining of venous graft vessels in rats. E: qPCR of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. Data are presented as the mean ± SD; *: compared with control group, p < 0.05. #: compared with sham group,

Application: IF/ICC    Species: Rat    Sample:

Fig. 6. A: PCNA immunofluorescence staining of venous graft vessels in rats. B, C: Western blot analysis of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. D: ICAM-1 immunofluorescence staining of venous graft vessels in rats. E: qPCR of α-SMA, PCNA, ICAM-1, VCAM-1, and vimentin in rat vein graft vessels. Data are presented as the mean ± SD; *: compared with control group, p < 0.05. #: compared with sham group,

2). HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury. CELLULAR & MOLECULAR BIOLOGY LETTERS, 2021 (PubMed: 34479471) [IF=8.3]

3). Novel Strategy for Isolation of Mice Bone Marrow–Derived Endothelial Cells (BMECs). Stem Cell Research & Therapy, 2020 (PubMed: 33941266) [IF=7.5]

4). Karyopherin α 2 promotes proliferation, migration and invasion through activating NF-κB/p65 signaling pathways in melanoma cells. LIFE SCIENCES, 2020 (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). Galectin-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation. JOURNAL OF CELLULAR PHYSIOLOGY, 2019 (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). Zinc attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury by activating Nrf2/GPX4 defense pathway. CNS Neuroscience & Therapeutics, 2021 (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). 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 (PubMed: 30419276) [IF=5.4]

8). Guang Chen Pi (the pericarp of Citrus reticulata Blanco's cultivars 'Chachi') inhibits macrophage-derived foam cell formation. JOURNAL OF ETHNOPHARMACOLOGY, 2022 (PubMed: 35489660) [IF=5.4]

9). 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 (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). Therapeutic effect and mechanism of 4‑phenyl butyric acid on renal ischemia‑reperfusion injury in mice. Experimental and Therapeutic Medicine, 2022 (PubMed: 35069825) [IF=2.7]

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