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Validated All-in-One™ qPCR Primer for VCAM1(NM_080682.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene is a member of the Ig superfamily and encodes a cell surface sialoglycoprotein expressed by cytokine-activated endothelium. This type I membrane protein mediates leukocyte-endothelial cell adhesion and signal transduction, and may play a role in the development of artherosclerosis and rheumatoid arthritis. Two alternatively spliced transcripts encoding different isoforms have been described for this gene.
Gene References into function
- Premature labor is associated with up-regulation of adhesion molecules in the lower uterine segment
- Soluble VCAM-1 is a very early marker of endothelial cell activation in cardiopulmonary bypass.
- significant increase in plasma levels between day 1 and day 5 of G-CSF-induced stem cell mobilization; possible effect on leukocyte-endothelial cell interactions
- Testosterone attenuates expression of vascular cell adhesion molecule-1 by conversion to estradiol by aromatase in endothelial cells: implications in atherosclerosis
- Elevated soluble CD40 ligand is related to the endothelial adhesion molecules in patients with acute coronary syndrome.
- Human mast cell progenitors use alpha4-integrin, VCAM-1, and PSGL-1, E-selectin for adhesive interactions with human vascular endothelium under flow conditions
- relation between glycemic control, hyperinsulinism and plasma concentration in patients with glucosse intolerance or NIDDM
- Results suggest that exogenous NO inhibits VCAM-1 expression via suppression of NF-kappaB through a cGMP-independent pathway.
- women with stage III and IV endometriosis had higher serum concentrations of soluble VCAM-1, lower serum concentration of soluble ICAM-1
- The tumor necrosis factor-alpha-stimulated redox-sensitive vascular cell adhesion molecule-1 selective signaling pathway in endothelial cells depends upon isoprenylcysteine carboxyl methyltransferase as a critical component.
- During leukocyte adhesion VCAM-1, ICAM-1, and activated moesin and ezrin clustered in an endothelial actin-rich docking structure that anchored and partially embraced the leukocyte containing other cytoskeletal components
- the preferential expression of VCAM-1 on the endothelium of femoral and iliac arteries in thromboangiitis obliterans
- VCAM-1/alpha4 integrin interactions mediate monocyte adhesion to human saphenous vein
- signal transduction pathways involved in rheumatoid arthritis synovial fibroblast interleukin-18-induced vascular cell adhesion molecule-1 expression
- VCAM-1 expression via effects on interferon regulatory factor-1 expression and activity
- E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy
- Downregulation of vcam-1 is associated with nodal metastasis in breast cancer
- Synchronized human hematopoietic progenitor cell adhesion fluctuates reversibly during cell cycle transit in ex vivo culture
- induction by tumor necrosis factor alpha
- Of the 10 candidate SNPs analyzed in this pilot study, the variant allele of the nonsynonymous SNP, VCAM1 G1238C, may be associated with protection from stroke.
- Relationship between pathological changes and the expression of vascular cell adhesion molecule-1 in the placenta of patients with pregnancy-induced hypertension complicated by intrauterine growth retardation
- VCAM1 stimulation by thrombin in endothelial cells is mediated by protein kinase C-delta-NF-kappa B and PKC-zeta-GATA signaling pathways
- VCAM1 expression is induced by p38-mediated TNFalpha and suppressed by JNK in human cells
- In adults with sickle cell disease, steady-state serum sVCAM-1 levels do not seem to reflect clinical disease severity, but may reflect bone marrow activity in SCD, underlying the pleiotropic nature of adhesion molecules in vivo.
- Strongly expressed in histological type II of rheumatoid arthritis.
- Crosslinking of CD44 on osteoblastic cells with specific antibodies augmented the expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1
- Endothelial cells have increased expression of VCAM-1, E-selectin, and ICAM-1 when exposed to sickle blood cells.
- VCAM-1-induced, Rac-dependent signaling plays a key role in the modulation of vascular-endothelial cadherin-mediated endothelial cell-cell adhesion and leukocyte extravasation.
- regulation of expression in osteoblasts by interleukin 13
- a novel role for the P2Y2 receptor in the p38- and Rho kinase-dependent expression of VCAM-1 that mediates the recruitment of monocytes by vascular endothelium associated with the development of atherosclerosis
- Soluble VCAM-1 markedly enhances phosphorylation of both p38 and focal adhesion kinase, but not ERK1/2, in endothelial cells, endothelial cell migration activity in vitro, and neovascularization in Matrigel in vivo.
- Extravasated and oxidized LDL in xanthoma adds to foam cell recruitment by activating tyrosine kinase and inducing adhesion of monocytes to dermal microvascular endothelial cells through VCAM-1 and E-selectin.
- Blood levels do not differ in normal and coronary artery disease patients.
- During infusion of triacylglycerol, PAI-1 increased to approximately 2.6 fold higher levels while tPA and adipsin were unaffected; changes in sVCAM-1 were significantly correlated with those seen for PAI-1.
- presence of vascular cell adhesion molecule (VCAM-1) in placental villi is specific to developmental stage, and it is decreased in fetal growth restriction which could be attributed to the uteroplacental deficiency
- Adrenomedullin and ACTH induce cell surface expression of adhesion molecules E-selectin, VCAM-1, and ICAM-1 on human umbilical vein endothelial cells.
- 11,12-EET analogues were synthesized and compared using a human endothelial cell based TNF-alpha-induced VCAM-1 expression assay.
- Novel androgen receptor/NF-kappaB mediated mechanism for VCAM-1 expression and monocyte adhesion operating in male endothelial cells that may represent an important unrecognized mechanism for the male predisposition to atherosclerosis.
- study demonstrates that overexpression of RORalpha1 and RORalpha4 inhibits TNF-alpha induced expression of VCAM-1 and ICAM-1 in human umbilical vein endothelial cells by inhibiting the NF-B signaling pathway
- sVCAM-1 was associated with dengue disease severity and the time post infection; a significant difference was found in the plasma levels of sVCAM-1 between dengue shock syndrome and dengue fever patients
- Insulin promotes VCAM-1 expression in endothelial cells through a p38MAP-kinase pathway, amplified by the PI3'-kinase blockage.
- even a short-term exposure of endothelial cells (ECs) to high glucose concentration leads to their activation associated with increased expression of adhesion molecules such as ELAM-1, VCAM-1 and ICAM-1.
- Expresson is reduced in treatment with methotrexate in bullous pemphigoid.
- Vascular cell adhesion molecule 1 may play an important role in asthma.
- Vascular cell adhesion molecule-1 may play an important inflammation-related role in plaque development.
- red blood cells from diabetic patients induced an increase in MCSF and VCAM1 expression in HUVEC cells, mediated by AGE-RAGE interaction
- P2Y2 nucleotide receptor mediates vascular cell adhesion molecule-1 expression through interaction with VEGF receptor-2
- Nifedipine decreases soluble VCAM-1
- a mechanism for ROS function in VCAM-1 activation of endothelial cell matrix metalloproteinase 2 and matrix metalloproteinase 9 during VCAM-1-dependent lymphocyte migration
- ICAM-1, VCAM-1, E-selectin and interleukin-6 expression are enhanced by glucose and regulated by poly(ADP-ribose) polymerase in human umbilical endothelial cells
- Cell adhesion to VCAM-1 mediated by very late antigen 4 was suppressed by monoclonal antibodies, dependent on reaction oxygen species.
- results suggest that in human tracheal smooth muscle cells (HTSMC), activation of p42/p44 MAPK, p38, JNK, and NF-kappaB pathways is essential for IL-1beta-induced VCAM-1 gene expression
- These findings indicate that signaling via PKCdelta-p38 kinase-linked cascade specifically induces expression of VCAM-1 in lung epithelium in response to TNF-alpha and that this effect is both functionally and clinically significant.
- Correlation between the vitreal levels of scatter factor and VCAM-1 was observed in diabetic patients.
- The VCAM-1 as multifunctional adhesion and signaling molecules has grown, , so has its recognition as potential therapeutic targets in human diseases.
- The data supports the hypothesis that gene modulation by IL-13 in ASM may be essential for the events leading to the development of allergic asthma.
- This is the first demonstration of expression of VCAM-1 on CD8+ cells; moreover, the CD8+VCAM-1+ cells show enhanced CD8+ cell noncytotoxic antiviral response activity that could have clinical importance in HIV infection.
- Direct implication of adhesion molecules in the pathogenesis or progression of type 2 diabetic retinopathy cannot be supported.
- VCAM-1 is mainly involved in the pathogenesis of hepatitis C-mixed cryoglobulinemia associated severe vasculitis.
- Genomic rearrangement on VCAM1 in arteriosclerosis was studied.
- Circulating sVCAM-1 correlates with residual renal function, LDL cholesterol & cardiac hypertrophy in CAPD patients. Besides being a marker of endothelial activation, sVCAM-1 play a role in LVH & heart failure by mediating immune cell-cell interaction.
- The induction of reactive oxygen species and VCAM-1 by AGEs in cultured human umbilical vein endothelial cells was specifically blocked by an anti-RAGE antibody
- The present study demonstrates for the first time, differential expression of mRNA and secretion for angiogenin and VCAM-1 from placental explants and trophoblasts in culture subjected to hypoxia
- VCAM-1 induction by CRP is mediated by PKC, p38MAPK, tyrosine kinase and the NF-kappaB-dependent signaling pathways in vascular endothelial cells.
- Anionic peptide factor/phosphatidylcholine particles promote the inhibition of VCAM1 in umbilical vein endothelial cells.
- anthrax lethal toxin enhanced cytokine-induced VCAM-1 expression and monocyte adhesion
- rhMIF induced VCAM-1 and ICAM-1 up-regulation in 12 hours via Src, PI3K, and NFkappaB
- data suggest a previously unappreciated role for VCAM-1 in esophageal squamous epithelial homeostasis and pathology
- PAR2-driven upregulation of VCAM-1 cell surface expression and the release of IL-8 and G-CSF from bronchial fibroblasts may be important in promoting neutrophilic airways inflammation.
- domain 4 of VCAM-1 plays a contrasting role when VCAM-1 is presented in solution or as a cell surface-expressed adhesive substrate
- ERK1/2 inhibition decreases VCAM-1 expression in TNFalpha-treated vascular endothelium cells.
- Use of icodextrin in peritoneal dialysis is not associatedd with increased VCAM1 plasma levels.
- important roles for VCAM-1 and Caveolin- 1 in the regulation of metastatic potential of gastric tumor cells
- as sVCAM-1 increased with exercise and during the recovery period, findings support the concept that sickle cell trait athletes might be at risk for microcirculatory disturbances and adhesive phenomena developing at rest and several hours after exercise
- CAM741 inhibits translocation of VCAM1 by interfering with correct insertion of its signal peptide into the translocon
- Gliclazide treatment reduces serum ICAM-1 levels in poorly controlled type 2 diabetic patients.
- persistently elevated, levels of sVCAM-1 throughout the various phases and types of the disease, suggests an important role in the immunopathological lesions of HFRS and is closely correlated to the severity of HFRS and the degree of kidney damage.
- Further analysis demonstrated that HDAC3 plays a significant role in the regulation of TNF-alpha-mediated VCAM-1 expression.
- LDL lipoprotein subunit L5 induces human umbilical vein endothelial cells (HUVEC) to express VCAM1.
- high levels of sICAM-1 and sVCAM-1, together with the presence of circulating endothelial cells in dengue hemorrhagic fever patients, provide further evidence of endothelium damage and activation in DHF patients
- A VCAM-1-mediated mechanism recruits leukocytes to the lymph nodes during inflammation.
- vascular cell adhesion molecules (sICAM-1 and sVCAM-1) and also P-selectin were higher in patients than healthy controls
- HOSCN induces E-selectin, ICAM-1, and VCAM-1 expression in HUVEC; HOSCN up-regulation of these adhesion molecules is transcriptionally mediated through a mechanism dependent upon activation of NFKB and constitutively suppressed by PI3K-Akt pathway.
- Increased plasma levels of VCAM-1 is associated with advanced stage of breast cancer
- Hemoglobin A1C in diabetics is positively associated with VCAM1 levels.
- ICAM-1 in cooperation with VCAM-1 are essential for monocyte adhesion by carbamylated low-density lipoprotein-activated human vascular endothelial cells in vitro.
- Positively associatted with age and tumor necrosis factor receptor 1 in type 2 diaabetes and insulin resistance.
- These findings reveal for the first time that TNF stimulation of adhesion molecules ICAM-1 and VCAM-1 in human endothelial cells occurs through the TNFR1 subtype and is mediated by the NF-kappaB pathway, but not the ERK, p38MAPK or JNK kinase pathways.
- These results suggest that in human tracheal smooth muscle cells, activation of p42/p44 MAPK, p38, and JNK pathways, at least in part, mediated through NF-kappaB, is essential for lipopolysaccharide-induced VCAM-1 gene expression.
- data indicate that HIV-1 Tat can modulate monocyte adhesiveness by increasing expression of adhesion molecules such as ICAM-1 and VCAM-1 via ROS- and NF-kappaB-dependent mechanisms in astrocytes
- High affinity interactions between the integrin alpha4beta1 on melanoma cells and VCAM-1 on activated endothelial cells may enhance the metastatic capacity of human beta2/beta3-negative melanoma cells.
- VCAM1 expression in LME cells and LFA-1 expression in HLA-DR15-positive monocytes were enhanced after combined culture of LME cells, HLA-DR15-positive monocytes and TRALI-inducing anti-HLA DR15 antibody-positive serum
- This report provides the first functional evaluation of VCAM1 promoter polymorphisms and establishes a hypothetical foundation for investigation of their role in the pathogenesis of VCAM1-associated diseases.
- lysophosphatidylcholine dose-dependently induced expression of vascular cell adhesion molecule-1 and P-selectin, accompanied by the activation of transcription factor nuclear factor kappaB.
- VCAM1 levels were positively correlated with C-reactive protein levels, indicating that increased level of oxidative stress marker, proinflammatory markers, and their downstream effectors adhesion molecules occur in type 2 DM.
- Cytokine-induced endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expressionwas inhibited by tecastemazole in a manner independent of H1 receptor antagonism.
- These findings indicate a novel role for C1INH in inhibition of vascular endothelial activation.
- The VCAM-1/very late activation antigen 4 adhesive system critically mediates endothelial progenitor cell adhesion to cultured rheumatoid arthritis fibroblasts and to rheumatoid arthritis synovial tissue.
- Patients withprimary hypertriglyceridemia as compared with control subjects showed significantly higher VCAM-1 (vascular cell adhesion molecule 1)
- circulating levels of adhesion molecules in correlated positively with the stage of kidney disease and with C-reactive protein
- soluble VCAM-1 levels increase only slightly in hemoculture positive neonatal sepsis.
- Pathophysiologically relevant homocysteine concentrations induce VCAM-1 expression through a prooxidant mechanism involving NF-kappaB.
- talin 1 is a versatile VLA-4 affinity regulator implicated in both spontaneous and chemokine-triggered rapid adhesions to VCAM-1.
- These results suggest that P2Y2R activation in salivary gland cells increases the EGFR-dependent expression of VCAM-1 and the binding of lymphocytes.
- our findings suggest that RCCs might exploit VCAM-1 overexpression for immune escape.
- Nicotine promotes VCAM1 expression on endothelial cells, shifting them toward a proatherosclerotic state.
- Women with endometriosis had increased peritoneal mRNA expression of RANTES and VCAM-1 during menstrual compared with luteal phase.
- In women with subsequent preeclampsia, sL-selectin and sVCAM-1 concentrations were significantly lower, whereas sE-selectin, sP-selectin and sICAM-1 levels were significantly higher, compared with controls at mid-pregnancy (p<0.05).
- OPG but not OPN stimulated a dose-dependent increase in the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin by endothelial cells in the presence of TNF-alpha
- in patients with cardiovascular disease or dyslipidemia, adiponectin was independently positively associated with serum HDL-cholesterol, sVCAM-1 (vascular cell adhesion molecule 1), female gender and negatively with hs-CRP (C reactive protein)
- sVCAM-1 level was higher in pp homozygotes of estrogen receptor alpha than PP homozygotes or Pp heterozygotes; higher in xx homozygotes than in XX homozygotes and Xx heterozygotes;and higher in px haplotype than in PX and Px haplotypes
- Cholestin reduces HCY-stimulated endothelial adhesiveness as well as downregulating intracellular ROS formation, NF-kappaB activation, and VCAM-1 expression in HAECs
- sVCAM-1 plays an arthritogenic role in the development of inflammatory arthritis in MRL-Fas(lpr) mice and may present an important target for therapeutic strategy of RA.
- There were no significant differences in the mean serum vascular cell adhesion molecule 1(VCAM1) concentration of women who developed pereclampsia and unaffected women.
- Iron, unlike interferon-gamma, does not appear to be involved in the regulation of ICAM-1 and VCAM-1 expression in cultured endometrial cells.
- Increased blood levels in rheumatoid arthritis are diminished after treatment with methotrexate.
- anlalysis of levels of circulating PIGF, SDF-1 and sVCAM-1 in patients with systemic lupus erythematosus
- CD106-positive human bone marrow stromal cell clones were less osteogenic and more adipogenic than CD106-negative clones.
- Diurnal variations in endogenous sVCAM-1 production in ST-segment elevation myocardial infarction patients might be related to an attenuated circadian secretion of melatonin.
- In cluster headache, sICAM-1, sVCAM-1 and sE-selectin showed an increasing trend in remission compared with the active period.
- Vascular cell adhesion molecule 1 expression is only blocked by the inhalational anesthetics and not by morphine.
- Endothelial cells express microRNA 126 (miR-126), which inhibits VCAM-1 expression.
- Urotensin-induced expression of TF and of VCAM-1/ICAM-1 was mediated through the Rho A-activation of the transcription factor, NF-kappaB
- Stromal sublayer of AA patients is characterized by low expression of Ang-1 and VCAM-1 genes and high VEGF expression compared to mean level of healthy donors.
- Increased VCAM-1 and P-selectin expression was associated with tricuspid regurgitant jet elevation regardless of etiology
- Homocysteine sensitizes HUVEC to the effect of inflammatory mediators thrombin and LPS, at least in part through VCAM-1 expression and function.
- Elevated VCAM-1 could serve as a marker for carotid stenosis but was not useful to identify plaques at risk for symptomatic conversion.
- Microparticle-associated vascular adhesion molecule-1 and tissue factor follow a circadian rhythm in healthy human subjects.
- key players involved in transmigration and invasion of MSCs are the endothelial phenotype, VCAM-1/VLA-4, beta1 integrins, MMP-2 secretion and cytokines.
- In prostate adenocarcinoma distant spread is more likely to occur in patients with high levels of VCAM and low levels of MMP-2.
- sVCAM-1 is a potential marker of hyperdynamic circulation, closely related to the different stages of liver cirrhosis.
- study reports that anthrax lethal toxin amplification of TNF-induced VCAM-1 expression is driven transcriptionally by the cooperative activation of NF-kappaB and IFN regulatory factor-1
- Baseline ICAM-1 and VCAM-1 are increased in initially healthy middle-aged men who develop cardiovascular disease during 6.6 years of follow-up.
- VEGF and VCAM-1 may participate in the pathogenesis of viral encephalitis.
- renal expression is upregulated in rapidly progressive glomerulonephritis
- The impact of pathophysiologically high insulin concentrations on cytokine-induced endothelial activation in human umbilical vein endothelial cells (HUVEC), was determined.
- Patients with inactive TA have elevated levels of sE-selectin, sVCAM-1, and sICAM-1 that might indicate persistent vasculopathy in clinically inactive disease.
- The expression of CD106, and osteogenic differentiation-related proteins and genes in human bone marrow (BM)-derived Mesenchymal stem cells, before and after differentiation.
- NF-kappaB, but not p38, is critical for TNF-alpha-induced expression of ICAM-1, VCAM-1 and E-selectin
- the gene expression of vascular cell adhesion molecule 1 (VCAM1) critically depends on [Ca2+]i oscillation frequency in the presence, as well as the absence, of histamine stimulation.
- TNF-alpha can play a crucial role in the immunopathogenesis of nephritis by the induction of CCL2, ICAM-1 and VCAM-1 expression via the activation of the intracellular MAPK signaling pathway, which may contribute to macrophage and lymphocyte infiltration
- High levels of sVCAM-1, associated with systemic tumour necrosis factor-alpha (TNFalpha) activity, were identified as a novel discriminator for systemic lupus erythematosus-related cardiovascular disease.
- VEGF, sVCAM-1, sICAM-1 and sE-selectin median levels were higher in hemodialysis patients compared to controls.
- Gb3 induces oxidative stress and up-regulates the expression of ICAM1, VACAM1 and selectin E in Fabry disease vascular endothelial cells.
- This independent association of postprandial triglycerides with sICAM-1 may indicate a particular impact of postprandial lipid metabolism on endothelial reaction.
- higher sICAM-1 and sVCAM-1 concentrations were independently associated with lower ankle-brachial index and peripheral arterial disease in blacks, but not in non-Hispanic whites
- Report the involvement of native TRPC3 proteins in ATP-dependent expression of VCAM-1 and monocyte adherence in coronary artery endothelial cells.
- correlations found between sVCAM-1, sICAM-1 and sELAM-1 and the presence of retinopathy suggest that cellular adhesion and neovascularization may be linked processes
- This study aimed to assess which cytokines regulate the expression of the adhesion molecule E-cadherin and the multi-functional protein beta-catenin, which plays a key role in cadherin-mediated anchoring in eosinophilic chronic rhinosinusitis.
- Data suggest that increased MIP-1alpha/beta production enhances multiple myeloma cell binding to stromal cells by VLA-4-VCAM-1 adhesion, forming a "vicious cycle" between MM cell adhesion to stromal cells and MIP-1 production via VLA-4-VCAM-1 interaction
- Presence is ssociated with regulation of ovarian cancer cell mesothelial invasion and metastatic progression and offers the possibility of novel therapeutic targets.
