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anti-Human SERPINE1 Antibodies:
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Human Polyclonal SERPINE1 Primary Antibody for ELISA, ICC - ABIN446967
Berard, Déglise, Alonso, Saucy, Meda, Bordenave, Corpataux, Haefliger: Role of hemodynamic forces in the ex vivo arterialization of human saphenous veins. in Journal of vascular surgery 2013
Show all 11 Pubmed References
Mouse (Murine) Polyclonal SERPINE1 Primary Antibody for ELISA (Detection), IHC (p) - ABIN491336
Weisberg, Albornoz, Griffin, Crandall, Elokdah, Fogo, Vaughan, Brown: Pharmacological inhibition and genetic deficiency of plasminogen activator inhibitor-1 attenuates angiotensin II/salt-induced aortic remodeling. in Arteriosclerosis, thrombosis, and vascular biology 2005
Show all 7 Pubmed References
Mouse (Murine) Monoclonal SERPINE1 Primary Antibody for Inhibition, ELISA (Detection) - ABIN491313
Cambier, Gline, Mu, Collins, Araya, Dolganov, Einheber, Boudreau, Nishimura: Integrin alpha(v)beta8-mediated activation of transforming growth factor-beta by perivascular astrocytes: an angiogenic control switch. in The American journal of pathology 2005
Show all 4 Pubmed References
Chimpanzee Polyclonal SERPINE1 Primary Antibody for IHC (p), ELISA - ABIN2476046
Faber, Lorimier, Sergysels: Cyclic haemodynamic and arterial blood gas changes during Cheyne-Stokes breathing. in Intensive care medicine 1990
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Mouse (Murine) Polyclonal SERPINE1 Primary Antibody for ELISA (Detection), WB - ABIN490932
Obi, Diaz, Ballard-Lipka, Roelofs, Farris, Lawrence, Henke, Wakefield: Low-molecular-weight heparin modulates vein wall fibrotic response in a plasminogen activator inhibitor 1-dependent manner. in Journal of vascular surgery. Venous and lymphatic disorders 2014
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Human Polyclonal SERPINE1 Primary Antibody for IHC, IHC (p) - ABIN4352929
Rice, Padilla, McLaughlin, Mathes, Ziemek, Goummih, Nakerakanti, York, Farina, Whitfield, Spiera, Christmann, Gordon, Weinberg, Simms, Lafyatis: Fresolimumab treatment decreases biomarkers and improves clinical symptoms in systemic sclerosis patients. in The Journal of clinical investigation 2015
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Human Monoclonal SERPINE1 Primary Antibody for FACS, IHC - ABIN969566
Oh, Olman, Benveniste: CXCL12-mediated induction of plasminogen activator inhibitor-1 expression in human CXCR4 positive astroglioma cells. in Biological & pharmaceutical bulletin 2009
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Mouse (Murine) Polyclonal SERPINE1 Primary Antibody for ELISA (Detection), IHC (p) - ABIN491337
Darehzereshki, Rubin, Gamba, Kim, Fraser, Huang, Billings, Mohammadzadeh, Wood, Warburton, Kaartinen, Lien: Differential regenerative capacity of neonatal mouse hearts after cryoinjury. in Developmental biology 2015
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Mouse (Murine) Monoclonal SERPINE1 Primary Antibody for ELISA (Capture), ELISA (Detection) - ABIN491254
Vayalil, Iles, Choi, Yi, Postlethwait, Liu: Glutathione suppresses TGF-beta-induced PAI-1 expression by inhibiting p38 and JNK MAPK and the binding of AP-1, SP-1, and Smad to the PAI-1 promoter. in American journal of physiology. Lung cellular and molecular physiology 2007
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Human Polyclonal SERPINE1 Primary Antibody for ELISA (Detection), IHC (p) - ABIN490950
Devin, Johnson, Eren, Gleaves, Bradham, Bloodworth, Vaughan: Transgenic overexpression of plasminogen activator inhibitor-1 promotes the development of polycystic ovarian changes in female mice. in Journal of molecular endocrinology 2007
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Hypoadiponectinemia and rising PAI-1 over time are early features of the cardiometabolic biomarker profile of women with recent gestational dysglycemia.
Positive PAI-1 membrane expression was significantly associated with local disease relapse of oral squamous cell carcinoma.
The 4G/4G, 4G/5G, and 5G/5G genotype frequencies were 40.0%, 46.4%, and 13.6% in the control group versus 31.4%, 52.0% and 16.6% in the IS group, respectively. The PAI-1 genotype dominant allele model was a risk factor for IS in patients with T2DM of Jinan, China.
results of study have not shown that individual genetic variation in PAI-1 is an independent variable that predispose same of children for renal scarring after first febrile urinary tract infection
upregulation of PAI-1 may be a critical mechanism underlying insufficient neurotrophic support and increased neurodegeneration associated with AD. Thus, targeting BDNF maturation through pharmacological inhibition of PAI-1 might become a potential treatment for AD.
CCL5, from endothelial cells, acts in a paracrine fashion on triple-negative breast cancer (TNBC) cells to enhance their migration, invasion, and metastasis. CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback loop. Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 signaling via the chemokine receptor, CCR5.
The present study shows that mean serum TSH and PAI-1 levels were higher in MetS cases as compared to healthy controls and even higher in MetS cases with SCH as compared to MetS cases without SCH. Thus, it can be summarized that in MetS with the presence of thyroid dysfunction, adipocytes behave abnormally and secrete various adipokines such as PAI-1 which in future may lead to thrombotic complication
Protease nexin-1 prevents growth of human B cell lymphoma via inhibition of sonic hedgehog signaling.
PAI-1 gene polymorphisms have roles in atherosclerotic diseases [review]
Decreased fibrinolytic activity increased, whereas PAI-1 4G/5G polymorphism did not influence venous thrombosis risk in this study.
The G-4G-C/A-5G-G PAI-1 haplogenotype may be a genetic marker of susceptibility for obesity and hypertriglyceridemia in Mexican children
The analysis of genotype coexistence revealed a higher incidence of the combination of the ACE II and the PAI-1 4G/4G genotypes in the control group (10.0 vs.5.9% in control group; p = 0.17). CONCLUSIONS: The obtained results suggest no apparent association between the ACE I/D, PAI-1 4G/5G polymorphisms and increased RM susceptibility in the analyzed Polish population.
Serum PAI-1 level at the time of traumatic brain injury may serve as a predictive biomarker of late pituitary dysfunction in mild traumatic brain injury patients.
The personalization of the patients' treatment using uPA/PAI-1 tumor levels allows the reversion of the well-known poor prognostic impact of high uPA/PAI-1 levels and strongly supports the use of this biomarker in clinical practice.
Data show that plasminogen activator inhibitor-1 (PAI-1) and chemokine CCL5 (CCL5) overexpression promoted cell proliferation and migration in breast cancer cells.
Multiple sclerosis patients were categorized as not cognitively impaired (NCI) and cognitively impaired (CI). The NCI group had a higher percentage of heterozygous subjects but no statistical differences were found between the CI and NCI group. Neuropsychological functioning did not correlate with plasma levels of PAI-1 or its genetic polymorphism. PAI-1 plasma levels were related to neurological impairment.
Results demonstrated that EMT could promote the secretion of PAI-1 in the triple negative breast cancer (TNBC) cells. TNBC-secreted PAI-1 could increase cell growth, migration and invasion, and the expression of EMT markers in the TNBC cell lines and xenograft mice model. Most importantly, PAI-1 expression is significantly elevated in the breast cancer tissues and associated with prognosis of patients with TNBC.
Plasma PAI-1 levels may be determined by the degree of obesity and triglyceride metabolic disorders. These factors correlate with a decreased LDL-particle size, increasing the risk of atherosclerosis.
In this meta-analysis, it was determined that PAI-1 polymorphism confers a genetic contribution to the development of recurrent spontaneous abortion.
The A allele and AA genotype of rs6092 in SERPINE 1 may protect against T2 diabetes, and have a protective effect on waist circumference, but a negative effect on Triglycerides in men, while may contribute to a lower HbA1c level in women.
The serpin PN1 is a feedback regulator of FGF signaling in germ layer and primary axis formation.
a highly dynamic endocardium in the regenerating zebrafish heart, with two key endocardial players, Serpine1 and Notch signalling, regulating crucial regenerative processes, is reported.
SERPINe1-derived 14-mer peptide and low molecular weight drugs targeting SERPINe1 (i.e. tannic acid, EGCG, tiplaxtinin) inhibited in vitro infections not only of viral haemorrhagic septicemia virus, but also of other fish rhabdoviruses.
X-ray crystal structure analysis of glycosylated fish PAI-1 confirmed the presence of an N-linked glycan in the gate region and a lack of glycan-induced structural changes.
PAI-1 functions as an inflammatory mediator that is rapidly deposited on the microvascular endothelium on ischemia-reperfusion injury and subsequently induces conformational changes in beta2 integrins of intravascularly rolling neutrophils.
endogenous RNA (Serpine1) controls the degradation of two miRNAs (miR-30b-5p and miR-30c-5p) in mouse fibroblasts
Results indicate that circadian locomotor output cycles kaput protein (CLOCK) overexpression triggers the formation of atherosclerotic plaques by directly upregulating plasminogen activator inhibitor 1 (PAI-1) expression.
In conclusion, we demonstrated that type 1 diabetes decreases accumulation and phagocytosis of macrophages at the damaged site during early bone repair after femoral bone injury through PAI-1 in female mice.
Findings indicate that plasminogen activator inhibitor-1 protects mice from hypertension-induced cardiac fibrosis by inhibiting the generation of active plasmin.
The effects of genetic alterations in PAI-1 expression, pharmacologic PAI-1 inhibition and recombinant PAI-1 on smooth muscle cell vitronectin (VN) expression were studied, and vascular VN expression in wild-type and PAI-1-deficient mice was assessed.
PAI-1 deficiency accelerates subchondral osteopenia after induction of osteoarthritis.
PAI-1 induces alveolar type II cell senescence through activating p53-p21-Rb pathway in fibrotic lung disease.
paracrine PAI-1 is involved in glucocorticoid-induced muscle wasting through the enhancement of muscle degradation in mice.
day-night feeding cycle is not a critical Zeitgeber for circadian rhythm of circulating PAI-1
PAI-1 is an in vivo target of the Pla protease in the lungs, and PAI-1 is a key regulator of the pulmonary innate immune response
the role of the antifibrinolytic protein plasminogen activator inhibitor-1 (PAI-1) in alcohol enhancement of experimental endotoxin-induced acute lung injury, is reported.
PAI-1 inhibitor PAI-039 prevents smooth muscle cell migration and neointimal hyperplasia.
Tongqiaohuoxue decoction exerted an anti-thrombotic effect through the regulation of PAI-1 and fibrinolysis.
PAI-1 plays a role in maintaining gastric mucosal organization in hypergastrinemia.
Olmesartan did not significantly affect PAI1 levels in this mouse model
BRD2 is involved in the modulation of neuroinflammatory responses through PAI-1 and via the regulation of epigenetic reader BET protein
Neutralization of the antifibrinolytic function of PAI-1 resolves skin fibrosis by limiting the extent of initial vascular injury and connective tissue inflammation.
These results suggest the critical physiological role of TRL4-Fyn interaction in the modulation of PAI-1-tPA axis in astrocytes during neuroinflammatory responses such as ischemia/reperfusion injuries.
In one pig population and in female pigs, SERPINE1 (serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1) was significantly associated with muscling, growth and fat accretion and in male animals with meat quality.
Data show that urokinase-type plasminogen activator (uPA) is only expressed in the cumulus cells of immature and in vitro matured cumulus-oocyte complexes (COCs), while uPA receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) are expressed in both the cumulus cells and the immature and in vitro matured oocytes.
Data suggest PAI1 plays key role in modulating chromaffin cell neurosecretory function. Evidence is presented that in chromaffin cells, PAI1 is targeted to storage vesicles and co-released with catecholamine upon secretagogue/stress stimulation.
the PI3K/Akt pathway acts as a negative regulator of PAI-1 expression in vascular endothelial cells, in part, through the downregulation of MAPK pathways
high glucose-induced plasminogen activator inhibitor-1 (PAI-1) expression in endothelial cells is mediated by NF-kappaB activation through the Rho/Rho-kinase pathway
FoxO1 inhibits PAI-1 expression through the inhibition of TGF-beta/Smad-mediated signaling pathways.
This gene encodes a member of the serine proteinase inhibitor (serpin) superfamily. This member is the principal inhibitor of tissue plasminogen activator (tPA) and urokinase (uPA), and hence is an inhibitor of fibrinolysis. Defects in this gene are the cause of plasminogen activator inhibitor-1 deficiency (PAI-1 deficiency), and high concentrations of the gene product are associated with thrombophilia. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
endothelial plasminogen activator inhibitor
, plasminogen activator inhibitor 1
, serine (or cysteine) proteinase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1
, serpin E1
, serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1
, PAI 1
, serine (or cysteine) proteinase inhibitor, clade E, member 1
, putative plasminogen activator inhibitor-1
, chemokine CCL-C25s
, plasminogen activator inhibitor 1-like
, Plasminogen activator inhibitor-1 precursor (PAI-1) (Endothelial plasminogen activator inhibitor) (PAI)
, nexin, plasminogen activator inhibitor type 1
, plasminogen activator inhibitor, type I
, serine (or cysteine) peptidase inhibitor, clade E, member 1
, serine (or cysteine) proteinase inhibitor, member 1
, plasminogen activator inhibitor I
, plasminogen activator inhibitor type 1
, plasminogen activator inhibitor, type 1
, plasminogen activator inhibitor-1