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Validated All-in-One™ qPCR Primer for PLAT(NM_000930.4) Search again
Product ID:
HQP013201
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
T-PA, TPA
Gene Description:
plasminogen activator, tissue type
Target Gene Accession:
NM_000930.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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.
Summary
This gene encodes tissue-type plasminogen activator, a secreted serine protease which converts the proenzyme plasminogen to plasmin, a fibrinolytic enzyme. Tissue-type plasminogen activator is synthesized as a single chain which is cleaved by plasmin to a two chain disulfide linked protein. This enzyme plays a role in cell migration and tissue remodeling. Increased enzymatic activity causes hyperfibrinolysis, which manifests as excessive bleeding; decreased activity leads to hypofibrinolysis which can result in thrombosis or embolism. Alternative splicing of this gene results in multiple transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- Steps and dynamics of disintegration and reorganization of fibrin networks during tissue-type plasminogen activator-induced clot lysis.
- mean transit time, the net quantitative turnover rate, and the sites of synthesis and catabolism
- PAI-1/ tPA imbalance is associated with myocardial infarction at young age in Japanese men.
- Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction. Genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.
- TPA & urokinase progressed to maximum levels in late pregnancy, but decreased in labor, favoring a coagulation state despite elevated D-dimer levels suggesting enhanced fibrinolysis.
- vWF and tPAag but not thrombomodulin in the present population are independent markers of atherosclerosis.
- Arsenite caused a decrease of t-PA mRNA level and a rise of both PAI-1 mRNA level and activity in microvascular endothelial cells, but not umbilical vein endothelial cells, suggesting a role in Blackfoot disease, a peripheral vascular occlusive disease.
- In a study of the differential role of UPA and TPA as inducers of fibronectin mRNA, TPA led to an increase of FN mRNA expression in early G1, led to FN assembly in the ECM, induced dimeric FN
- Tissue-type plasminogen activator is stored in Weibel-Palade bodies in endothelial cells
- role of the plasminogen activator and matrix metalloproteinase systems in matrix remodeling in the ovary
- Tissue plasminogen activator as a key effector in neurobiology and neuropathology. Review.
- tPA is induced by oncostatin M in lung tumor cells
- interactions between the fibrinolytic and renin-angiotensin systems play an important role in the genetic architecture of plasma t-PA
- upregulation of PAI-1, uPA, and tPA after long-term LDL exposure seems to be mediated by a delayed PKC activation associated with an increased PA inhibitory activity
- The interactions between NSP and t-PA were distinct from those between plasmin and NSP, suggesting that the physiologic effect of t-PA-NSP interactions may be more complex than previously thought.
- Cloning and identification of human tissue-type plasminogen activator gene.
- Calcium-regulated secretion of tissue-type plasminogen activator in vascular endothelial cells.
- amino acids critical for tPA-annexin A2 interaction
- hypoxia decreased tissue plasminogen activator in both normal peritoneal fibroblasts and adhesion fibroblasts
- reactive hyperemia stimulates t-PA release; that relationship is altered when endothelium is dysfunctional. Release of t-PA is independent of adenosine or products of muscarinic stimulation and may be related to the activity of the kininogen/kinin system
- Recombinant tissue plasminogen activator (alteplase)is effective for restoration of function to occluded central venous catheters in a pediatric population with thrombosis
- The possible influence of the Alu-repeat polymorphism on t-PA release was evaluated after a venous occlusion test in venous occlusion.
- Tetranectin binds to this protein and hepatocyte growth factor.
- results show that the NH(2)-terminal part of PrP(c) spanning amino acids 23-110 (PrP23-110) together with low molecular weight heparin stimulates t-PA mediated plasminogen activation in vitro
- tPA and plasma kallikrein-mediated uPA activation and tPA release contribute to endogenous fibrinolytic or thrombolytic mechanisms.
- In normal conditions and in the presence of IL-1beta, cathepsin B is involved in the activation of plasminogen activator in osteoblasts.
- These results suggest that the recombinant kringle domain of tissue-type plasminogen activator (t-PA) is a selective inhibitor of endothelial cell growth and identifies this molecule as a novel anti-angiogenic agent.
- Dengue virus infection significanlty increased production of tissue plasminogen activator (tPA) in primary isolated endothelial cells, human umbilical cord veins cells, and a human microvascular endothelial cell line
- evidence to support the hypothesis that p63 is the functional tPA binding site on VSMC
- TAFIa inhibited lysis of model thrombi and plasma clots by uPA, scuPA and tPA, which could be partially overcome by plasminogen, consistent with TAFIa exerting its effect through modifying the binding of plasminogen and tPA to fibrin.
- the catalytic domain of tissue-type plasminogen activator is distorted by plasminogen activator inhibitor-1, leading to the formation of stable serpin-proteinase complexes
- High concentration of plasma tPA was an independent marker for poor prognosis in patients with ovarian cancer.
- in response to T beta 4 stimulation, AP-1 activity increases to enhance PAI-1 transcription through its unique AP-1-like element at -59 to -52 in the PAI-1 promoter.
- A coconut oil-based diet lowers postprandial t-PA antigen concentration.
- anti-tPA antibodies specifically interacting with the catalytic domain of tPA can be found in patients with antiphospholipid syndrome, representing a possible cause of hypofibrinolysis.
- t-PA antigen concentration (P =.001), fibrinogen and time on dialysis prior to transplantation (P <.05) were positive independent predictors of carotid intima media thickness in kidney transplantation.
- t-PA mediated plasminogen activation involves prion-protein fragment PrP23-110 lysine clusters
- Adenosine deaminase and Plasminogen bind simultaneously to CD26 in a ternary complex that stimulates the Pg activation by its physiologic activators.
- Neuronal depolarization induces a release of t-PA. This release of t-PA is sensitive to exocytosis inhibition and calcium chelation. Released t-PA modulates NMDA receptor signaling.
- There is a basal net release of t-PA across the human cerebral vascular bed and sympathoadrenal activation induces a local regulated release of t-PA.
- All plasminogen activators tested bearing kringle domains bind to PrP23-110; the lysine-binding site of kringle 2 that is unique to t-PA appears to mediate the specific stimulation of plasminogen activation by the cellular prion protein
- tissue plasminogen activator and neuroserpin are widely expressed in the human central nervous system
- arginine 260 is necessary for both tPA-induced cleavage of the ATD of NR1 and tPA-induced potentiation of NMDA receptor signaling
- This review focuses on the role of tissue plasminogen activator expression and secretion related to the structural and functional changes of hippocampal synapses during late-phase long term potentiation, in the context of long-term memory.
- The major determinant for the local availability of active tPA is the capacity of the endothelium to release tPA rather than the arterial input of PAI-1 or tPA.
- sesamol increased the production of uPA and tPA significantly and also up-regulated the mRNA expressions of these proteins.
- kringle domain (TK1-2) of human t-PA inhibits the tumor growth by suppression of angiogenesis without interfering with fibrinolysis
- tPA gene expression is induced by lysophosphatidylcholine through CRE-dependent mechanism
- This review explores the profound effects of the fibrin-modifying protease T-PA on neurons and glial cells in the brain and its capability of altering the development and severity of ischemic stroke.
- identification of a previously undescribed kappaB site in the t-PA gene promoter that influences t-PA expression in neuronal cells
- The levels of P-selectin, tPA antigen, and PAI-1 activity were all significantly higher in stroke patients compared with controls.
- no association between t-PA genotype and venous thromboembolism.
- The Tissue Plasminogen Activator mRNA level was decreased in pericyte cocultures with human brain microvascular endothelial cells.
- Elevated plasma levels in, and therefore a marker for cancers.
- neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism show significant association with ischemic stroke, but the tPA CC/PAI-1 4G4G genotype combination may have a protective effect
- Some of the plasmin-reactive anticardiolipin antibodies in antiphospholipid syndrome patients may bind to tPA
- "Morphologically normal tissues" adjacent to carcinomas present abnormal t-PA activity that is associated with the degree of tumor progression.
- the TPA -7351C/T polymorphism may have a role in lacunar stroke [letter]
- one of the important proteolysis factors in the pathogenesis of pulpal inflammation
- Regulation of endogenous tissue-type plasminogen activator expression is modulated by the -7351C>T enhancer polymorphism.
- The analysis of PLAT and LCN2 transcripts in 12 samples obtained through EUS-guided FNA from patients with pancreatic adenocarcinoma showed significantly increased expression levels in comparison with those found in normal tissues.
- genetic variation of the t-PA locus is unlikely to have a major influence on acute t-PA release in subjects with established CHD
- The prevalence of anti-t-PA antibodies is high in inflammatory bowel disease patients. Binding sites are the catalytic or kringle-2 domains of t-PA.
- TNF-alpha impairs fibrinolytic capacity in vascular endothelial cells by a NF-kappaB and p38 MAPK-dependent suppression of t-PA
- the G-T haplotype at rs7007329-rs8178750 of the tPA gene may have a role in development of ischemic stroke
- Changes in blood viscosity were determined with the recombinant tissue plasminogen activator alteplase.
- In a Cox regression model, a tPA concentration >19 ng/mL was independently associated with mortality in patients with acute myocardial infarct
- nicotine stimulates bone matrix turnover by increasing production of tPA and MMP-1, 2, 3, and 13, thereby tipping the balance between bone matrix formation and resorption toward the latter process
- These results support the idea that the interplay between the renin-angiotensin, bradykinin, and fibrinolytic systems might play an important role in t-PA and PAI-1 biology.
- the D polymorphic allele could be associated with susceptibility to generalized aggressive periodontitis in Turkish subjects
- t-PA release is Galphaq-, PLC-beta-, IP3-, and 5,6-EET-dependent in thrombin-stimulated microvascular endothelial cells.
- PLAT response to venous occlusion was independently associated with patient age at onset of first ST-elevation myocardial infarction
- Fibrinogen and fibrin modulate the activity of tPA differently in regard to their activation of plasminogen and inhibition by PAI-1
- Human t-PA promoter confers brain-derived neurotrophic factor-responsiveness in transfected mouse primary cortical neurons.
- In thyroid cells, plasminogen activators are regulated via MAPK and protein kinase c-beta pathways.
- postprandial glucagon was independently associated with PAI-1/t-PA in normal glucose tolerance
- Plasminogen activator inhibitor type 1 genotypes are not associated with susceptibility to chronic periodontitis in Turkish subjects.
- Regionally deficient tissue plasminogen activator expression in microvessel endothelium contributes to impaired endogenous fibrinolysis and microvascular ischemia in diabetic neuropathy.
- Analysis of TPA gene's Alu-repeat insertion/deletion (I/D) polymorphism the PCOS patients with genotype II had lowers total cholesterol and LDL-cholesterol levels.
- heart rate recovery after exercise was inversely correlated with plasminogen activator inhibitor 1 (PAI-1) activity, tissue plasminogen activator (t-PA) antigen, and fibrinogen
- No correlation between tPA polymorphism and D allele carriage in hepatopulmonary syndrome.
- TPA DD/PAI-1 4G4G genotype combination has reached a borderline significance for reduced risk for multiple sclerosis
- IL-8 induces imbalances between nitric oxide and endothelin-1, and also between plasminogen activator inhibitor-1 and tissue-type plasminogen activator in cultured endothelial cells
- elevated in polycystic ovary syndrome
- tPA induces LRP-1 tyrosine phosphorylation, which in turn facilitates the LRP-1-mediated recruitment of beta1 integrin and downstream ILK signaling, thereby leading to myofibroblast activation.
- data demonstrate that local elevation of plasminogen activator activity in the lungs improves host defense against severe gram-negative pneumonia and sepsis
- IL-1beta stimulates uPA but not tPA production via activation of NFkappaB and tyrosine phosphorylation, and also secretion of the enzyme, and that the uPA/plasmin system appears to be involved in inflammation in human dental pulp.
- These results provide new insights into the mechanism of a tPA-induced, LRP1-mediated gating mechanism for NMDA receptors.
- there is a functional Sp1-binding element in the t-PA promoter controlling quercetin induction via the p38 MAPK pathway
- In lymphocytes obtained from healthy persons more t-PA and PAI-1 was detected than in lymphocytes from patients with chronic lymphoid leukemia
- prolonged laparoscopic surgery causes a decreased fibrinolytic activity in the peritoneum due to decreased tPA levels.
- Our results show an impaired adrenergic-stimulated t-PA release among essential hypertensive patients, probably mediated via a reduced NO availability.
- tPA may lead to an opening of the blood-brain barrier (BBB) under non-ischemic conditions and have an additional effect on the ischemia-induced BBB disruption.
- Investigation of PAI-1 gene 4G/5G polymorphism frequency and TPA enzyme activity in patients with acute stroke reports that there is no direct relation.
- PAI-2 can inhibit cell-bound tPA activity in vitro and thus prevent plasmin formation
- function of the tPA during diapedesis of monocytes through brain endothelial barrier; monocytes induce the release of tPA by brain endothelial cells; tPA and ERK1/2 control the breakdown of the tight junction protein occludin.
- relationship between exocytosed, membrane-retained tPA and PAI-1, which would modulate cell surface-associated fibrinolytic potential.
- t-PA and PAI-1 levels are determined by both genetic loci of the fibrinolytic and renin-angiotensin systems and other factors often associated with cardiovascular disease
- Pregnancy is associated with major perturbations of endogenous fibrinolytic capacity with an overwhelming increase in plasma PAI-1 concentrations and an inadequate release of active t-PA
- Prolonged high laminar shear stress suppresses endothelial t-PA expression and may therefore contribute to the enhanced risk of arterial thrombosis in hypertensive disease.
- TPA is expressed in cancer cells. With its receptor annexin II on endothelial surface, it regulates intravascular fibrin deposition. Review.