A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.
A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)
The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.
A deficiency of blood coagulation factor V (known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as Owren's disease or parahemophilia. It varies greatly in severity. Factor V deficiency is an autosomal recessive trait. (Dorland, 27th ed)
An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
Laboratory tests for evaluating the individual's clotting mechanism.
Three or more consecutive spontaneous abortions.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.
Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.
Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Formation and development of a thrombus or blood clot in the blood vessel.
A member of the serpin family of proteins that is found in plasma and urine. It is dependent on heparin and is able to inhibit activated PROTEIN C; THROMBIN; KALLIKREIN; and other SERINE ENDOPEPTIDASES.
The formation or presence of a blood clot (THROMBUS) within a vein.
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
An individual in which both alleles at a given locus are identical.
A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.
An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
A pulmonary surfactant associated protein that plays a role in alveolar stability by lowering the surface tension at the air-liquid interface. It is a membrane-bound protein that constitutes 1-2% of the pulmonary surfactant mass. Pulmonary surfactant-associated protein C is one of the most hydrophobic peptides yet isolated and contains an alpha-helical domain with a central poly-valine segment that binds to phospholipid bilayers.
Simultaneous resistance to several structurally and functionally distinct drugs.
The capacity of an organism to defend itself against pathological processes or the agents of those processes. This most often involves innate immunity whereby the organism responds to pathogens in a generic way. The term disease resistance is used most frequently when referring to plants.
A species of gram-negative, fluorescent, phytopathogenic bacteria in the genus PSEUDOMONAS. It is differentiated into approximately 50 pathovars with different plant pathogenicities and host specificities.
The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
Those components of an organism that determine its capacity to cause disease but are not required for its viability per se. Two classes have been characterized: TOXINS, BIOLOGICAL and surface adhesion molecules that effect the ability of the microorganism to invade and colonize a host. (From Davis et al., Microbiology, 4th ed. p486)
Diseases of plants.
Proteins found in any species of bacterium.
Proteins that originate from plants species belonging to the genus ARABIDOPSIS. The most intensely studied species of Arabidopsis, Arabidopsis thaliana, is commonly used in laboratory experiments.
A plant genus of the family BRASSICACEAE that contains ARABIDOPSIS PROTEINS and MADS DOMAIN PROTEINS. The species A. thaliana is used for experiments in classical plant genetics as well as molecular genetic studies in plant physiology, biochemistry, and development.

Synergistic effects of prothrombotic polymorphisms and atherogenic factors on the risk of myocardial infarction in young males. (1/111)

Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C --> T, factor V (F V) nt 1691G --> A (F V Leiden), and factor II (F II) nt 20210 G --> A on the risk of myocardial infarction. In the present study, we analyzed the effect of these prothrombotic polymorphisms, as well as apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and hypercholesterolemia, on the risk of myocardial infarction in young males. We conducted a case-control study of 112 young males with first acute myocardial infarction (AMI) before the age of 52 and 187 healthy controls of similar age. The prevalences of heterozygotes for F V G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among cases and controls, respectively). In contrast, the prevalence of MTHFR 677T homozygosity and the allele frequency of Apo E4 were significantly higher among patients (24.1% v 10.7% and 9.4% v 5.3% among cases and controls, respectively). Concomitant presence of hypertension, hypercholesterolemia, or diabetes and one or more of the four examined polymorphisms increased the risk by almost ninefold (odds ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5) and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed simultaneously by a logistic model, the combination of prothrombotic and Apo E4 polymorphisms with current smoking increased the risk 25-fold (OR = 24.7; 95% CI, 7.17 to 84.9). The presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of AMI, as was recently found in a similar cohort of women.  (+info)

Thrombophilia as a multigenic disease. (2/111)

BACKGROUND AND OBJECTIVE: Venous thrombosis is a common disease annually affecting 1 in 1000 individuals. The multifactorial nature of the disease is illustrated by the frequent identification of one or more predisposing genetic and/or environmental risk factors in thrombosis patients. Most of the genetic defects known today affect the function of the natural anticoagulant pathways and in particular the protein C system. This presentation focuses on the importance of the genetic factors in the pathogenesis of inherited thrombophilia with particular emphasis on those defects which affect the protein C system. INFORMATION SOURCES: Published results in articles covered by the Medline database have been integrated with our original studies in the field of thrombophilia. STATE OF THE ART AND PERSPECTIVES: The risk of venous thrombosis is increased when the hemostatic balance between pro- and anti-coagulant forces is shifted in favor of coagulation. When this is caused by an inherited defect, the resulting hypercoagulable state is a lifelong risk factor for thrombosis. Resistance to activated protein C (APC resistance) is the most common inherited hypercoagulable state found to be associated with venous thrombosis. It is caused by a single point mutation in the factor V (FV) gene, which predicts the substitution of Arg506 with a Gln. Arg506 is one of three APC-cleavage sites and the mutation results in the loss of this APC-cleavage site. The mutation is only found in Caucasians but the prevalence of the mutant FV allele (FV:Q506) varies between countries. It is found to be highly prevalent (up to 15%) in Scandinavian populations, in areas with high incidence of thrombosis. FV:Q506 is associated with a 5-10-fold increased risk of thrombosis and is found in 20-60% of Caucasian patients with thrombosis. The second most common inherited risk factor for thrombosis is a point mutation (G20210A) in the 3' untranslated region of the prothrombin gene. This mutation is present in approximately 2% of healthy individuals and in 6-7% of thrombosis patients, suggesting it to be a mild risk factor of thrombosis. Other less common genetic risk factors for thrombosis are the deficiencies of natural anticoagulant proteins such as antithrombin, protein C or protein S. Such defects are present in less than 1% of healthy individuals and together they account for 5-10% of genetic defects found in patients with venous thrombosis. Owing to the high prevalence of inherited APC resistance (FV:Q506) and of the G20210A mutation in the prothrombin gene, combinations of genetic defects are relatively common in the general population. As each genetic defect is an independent risk factor for thrombosis, individuals with multiple defects have a highly increased risk of thrombosis. As a consequence, multiple defects are often found in patients with thrombosis.  (+info)

Factor V Leiden and antibodies against phospholipids and protein S in a young woman with recurrent thromboses and abortion. (3/111)

We describe the case of a 39-year-old woman who suffered two iliofemoral venous thromboses, a cerebral ischemic infarct and recurrent fetal loss. Initial studies showed high levels of antiphospholipid antibodies (APAs) and a moderate thrombocytopenia. After her second miscarriage, laboratory diagnosis revealed that the woman was heterozygous for the factor V Leiden mutation and had a functional protein S deficiency as well as anti-protein S and anti-beta 2-glycoprotein I antibodies. The impairment of the protein C pathway at various points could well explain the recurrent thromboses in the patient and supports the role of a disturbed protein C system in the pathophysiology of thrombosis in patients with APAs.  (+info)

Simultaneous detection of FV Q506 and prothrombin 20210 A variation by allele-specific PCR. (4/111)

BACKGROUND AND OBJECTIVE: Factor V Leiden is the most important risk factor for hereditary thromboembolism, whereas the mutation in the 3'-untranslated region of the prothrombin gene seems to be only a mild risk factor for thrombotic events. On the other hand the factor V mutation (Arg 506) is frequently coinherited with the prothrombin 3'-untranslated region G20210A variant and there is increasing evidence that the co-segregated prothrombin variant is an additional risk factor for venous thromboembolism, contributing to thrombotic manifestations. A rapid, simple and cost-effective screening method is, therefore, required for the detection of both factor V Leiden and the prothrombin variant A20210G. DESIGN AND METHODS: Eighty-eight patients were enrolled in this study. Forty-four had a previously identified factor V and/or prothrombin mutation, the remaining 44 patients served as negative controls. A multiplex allele specific oligonucleotide PCR was established for the simultaneous detection of the two genetic risk factors for thrombophilia. To test the specificity of the simultaneous ASO PCR approach, the mutated and physiological factor V and prothrombin amplification products were sequenced. RESULTS: The factor V Leiden mutation and the prothrombin variant were correctly identified in all of 44 patients with known mutations. Furthermore the test was able to detect the mutated factor V and the II variant alone, as well as in the cosegregated pattern. Five patients with a homozygous pattern of factor V Leiden or prothrombin variant were also correctly identified. The sensitivity of the test is therefore 100%. In none of the 44 control cases were false positive results seen. INTERPRETATION AND CONCLUSIONS: The ASO PCR test is a rapid, simple and cost-effective screening test for thrombophilia.  (+info)

Coagulation factors II, V, VII, and X, prothrombin gene 20210G-->A transition, and factor V Leiden in coronary artery disease: high factor V clotting activity is an independent risk factor for myocardial infarction. (5/111)

Increased levels of hemostatic factors and genetic mutations of proteins involved in coagulation may play a role in the pathogenesis of coronary artery disease. We investigated clotting activity of factors II (FII:C), V (FV:C), VII (FVII:C), and X (FX:C), the prothrombin gene 20210G-->A transition, and the factor V Leiden mutation in 200 survivors of myocardial infarction and in 100 healthy controls. FV:C (P<0.0001) and FVII:C (P<0.0001) were found to be independent risk factors for myocardial infarction. High FV:C or high FVII:C combined with smoking or arterial hypertension increased the relative risk for myocardial infarction up to 50-fold. One of 177 patients (0.6%) and 4 of 89 controls (4.5%) had the prothrombin 20210 AG genotype. Eleven of 177 patients (6.2%) and 6 of 89 controls (6.7%) were heterozygous for the factor V Leiden mutation. No homozygous carrier for these mutations was found. Neither the prothrombin gene 20210G-->A transition (odds ratio [OR], 0.1; 95% confidence interval [CI], 0.01 to 1.1) nor the factor V Leiden mutation (OR, 1.0; 95% CI, 0.4 to 2.8) were associated with an increased relative risk for myocardial infarction. In conclusion, our data indicate that neither the prothrombin gene 20210G-->A transition nor the factor V Leiden mutation are risk factors for myocardial infarction. High FVII:C was confirmed to be an independent risk factor for myocardial infarction. Moreover, we describe for the first time that high FV:C is an independent risk factor for myocardial infarction.  (+info)

Risk of venous thromboembolism and clinical manifestations in carriers of antithrombin, protein C, protein S deficiency, or activated protein C resistance: a multicenter collaborative family study. (6/111)

Deficiencies of antithrombin (AT), protein C (PC) or protein S (PS), and activated protein C resistance (APCR) are very well-established coagulation defects predisposing to venous thromboembolism (VTE). We performed a retrospective cohort family study to assess the risk for VTE in individuals with AT, PC, or PS deficiency, or APCR. Five hundred thirteen relatives from 9 Italian centers were selected from 233 families in which the proband had had at least 1 episode of VTE. We calculated the incidence of VTE in the whole cohort and in the subgroups after stratification by age, sex, and defect. The overall incidence of VTE (per 100 patient-years) in the group of relatives was 0.52. It was 1.07 for AT, 0.54 for PC, 0.50 for PS, 0.30 for APCR, and 0.67 in the group with a double defect. The incidence was associated with age, but not with sex. The mean age at onset was between 30 and 40 years for all the coagulation defects. Women had the peak of incidence in the age range of 21 to 40 years, earlier than men. The lifetime risk for VTE was 4.4 for AT versus APCR, 2.6 for AT versus PS, 2.2 for AT versus PC, 1.9 for PC versus APCR, and 1.6 for PS versus APCR. AT deficiency seems to have a higher risk for VTE than the other genetic defects. There is a relation between age and occurrence of thrombosis for both men and women. The latter had the peak of incidence earlier than the former.  (+info)

Activated protein C resistance: effect of platelet activation, platelet-derived microparticles, and atherogenic lipoproteins. (7/111)

Plasma and platelet factor Va represent different substrates for activated protein C (APC). In this study, we have measured platelet-dependent APC resistance and the effect of aspirin and a platelet glycoprotein IIbIIIa antagonist (GR144053F) on this phenomenon. In platelet rich plasma (PRP), progressive APC resistance was observed with increasing platelet activation. APC sensitivity ratios of 1.8, 1.7, and 1.4 were observed after platelet activation with thrombin receptor activating peptide (TRAP), collagen, and A23187, respectively. Ultracentrifugation at 77,000g for 1 hour abolished APC resistance indicating that the phenotype is associated exclusively with the platelet membrane. APC resistance was not observed in the presence of phosphatidylcholine-phosphatidylserine (PCPS) vesicles or purified human plasma lipoproteins. APC resistance was observed in the presence of platelet-derived microparticles, but to a lesser degree than that in the presence of activated platelets. The platelet-dependent APC resistance phenotype was also observed when endogenous APC was generated by Protac (American Diagnostica, Inc, Greenwich, CT). In vitro inhibition of platelet activation with aspirin had no effect, but the fibrinogen receptor antagonist, GR144053F, inhibited platelet-dependent APC resistance. These results indicate that platelet activation results in an APC-resistant phenotype comparable to that observed in the plasma of patients with factor V gene mutations affecting critical APC cleavage sites. This suggests that platelet activation at the site of endothelial damage downregulates a critical natural anticoagulant mechanism. The antithrombotic effect of aspirin may be due to an indirect effect on platelet-dependent APC resistance with reduced platelet retention within a developing thrombus. The more potent antithrombotic effect of glycoprotein IIbIIIa antagonists may in addition be the result of reduced platelet factor Va expression and modulation of the platelet-dependent APC resistance phenotype.  (+info)

A possible role for activated protein C resistance in patients with first and second trimester pregnancy failure. (8/111)

Thrombophilia was recently suggested as a possible factor in recurrent pregnancy losses. We studied prospectively 125 patients (mean age 31.4 +/- 5.6 years) with one or more first or second trimester pregnancy losses for the prevalence of activated protein C resistance (APCR). Proteins C and S antigens, antithrombin III, anticardiolipin, and lupus anti-coagulant were also evaluated. Patients with uterine malformations, hormonal abnormalities, chromosomal translocations and infectious causes were excluded. A control group of 125 women with no past fetal loss were matched with the study group. Whenever the APC-sensitivity ratio (APC-SR) was +info)

APC resistance can be caused by genetic or acquired factors and can lead to a range of clinical presentations, including:

1. Hereditary bleeding disorders: Familial APC resistance is caused by mutations in the APC gene and can result in severe bleeding, especially during childhood.
2. Acquired APC resistance: This can occur due to certain medical conditions, such as liver disease, sepsis, or cancer, which can impair APC function.
3. Drug-induced APC resistance: Certain medications, like anticoagulants, can reduce APC activity and lead to APC resistance.

Diagnosis of APC resistance typically involves testing for APC activity in the blood, as well as genetic analysis to identify mutations in the APC gene. Treatment options for APC resistance depend on the underlying cause and may include:

1. Fresh frozen plasma (FFP): FFP can be used to replace missing or deficient APC in the blood.
2. Recombinant APC: This is a synthetic version of APC that can be used to replace missing or deficient APC.
3. Anticoagulants: These medications can help prevent blood clots and reduce the risk of thrombotic events.
4. Platelet inhibitors: These medications can help prevent platelet aggregation, which can contribute to bleeding.

Overall, APC resistance is a rare but important condition that can affect blood coagulation and increase the risk of bleeding or thrombotic events. Prompt diagnosis and appropriate treatment are essential to manage the condition effectively and prevent complications.

Word origin: [Latin] proteinus, "protein" + C, "deficiency"

There are several types of thrombophilia, including:

1. Factor V Leiden: This is the most common inherited thrombophilia and is caused by a mutation in the Factor V gene.
2. Prothrombin G20210A: This is another inherited thrombophilia that is caused by a mutation in the Prothrombin gene.
3. Protein C and S deficiency: These are acquired deficiencies of protein C and S, which are important proteins that help to prevent blood clots.
4. Antiphospholipid syndrome: This is an autoimmune disorder that causes the body to produce antibodies against phospholipids, which can lead to blood clots.
5. Cancer-associated thrombophilia: This is a condition where cancer patients are at a higher risk of developing blood clots due to their cancer and its treatment.
6. Hormone-related thrombophilia: This is a condition where hormonal changes, such as those that occur during pregnancy or with the use of hormone replacement therapy, increase the risk of blood clots.
7. Inherited platelet disorders: These are rare conditions that affect the way platelets function and can increase the risk of blood clots.
8. Anti-cardiolipin antibodies: These are autoantibodies that can cause blood clots.
9. Lupus anticoagulant: This is an autoantibody that can cause blood clots.
10. Combined genetic and acquired risk factors: Some people may have a combination of inherited and acquired risk factors for thrombophilia.

Thrombophilia can be diagnosed through various tests, including:

1. Blood tests: These tests measure the levels of certain proteins in the blood that are associated with an increased risk of blood clots.
2. Genetic testing: This can help identify inherited risk factors for thrombophilia.
3. Imaging tests: These tests, such as ultrasound and venography, can help doctors visualize the blood vessels and look for signs of blood clots.
4. Thrombin generation assay: This test measures the body's ability to produce thrombin, a protein that helps form blood clots.
5. Platelet function tests: These tests assess how well platelets work and whether they are contributing to the development of blood clots.

Treatment for thrombophilia usually involves medications to prevent or dissolve blood clots, as well as measures to reduce the risk of developing new clots. These may include:

1. Anticoagulant drugs: These medications, such as warfarin and heparin, are used to prevent blood clots from forming.
2. Thrombolytic drugs: These medications are used to dissolve blood clots that have already formed.
3. Compression stockings: These stockings can help reduce swelling and improve blood flow in the affected limb.
4. Elevating the affected limb: This can help reduce swelling and improve blood flow.
5. Avoiding long periods of immobility: This can help reduce the risk of developing blood clots.

In some cases, surgery may be necessary to remove a blood clot or repair a damaged blood vessel. In addition, people with thrombophilia may need to make lifestyle changes, such as avoiding long periods of immobility and taking regular breaks to move around, to reduce their risk of developing blood clots.

Overall, the prognosis for thrombophilia is generally good if the condition is properly diagnosed and treated. However, if left untreated, thrombophilia can lead to serious complications, such as pulmonary embolism or stroke, which can be life-threatening. It is important for people with thrombophilia to work closely with their healthcare provider to manage the condition and reduce the risk of complications.

Protein S is a vitamin K-dependent protein that is produced in the liver and circulates in the blood. It works by inhibiting the activity of thrombin, a clotting factor that helps to form blood clots. In people with protein S deficiency, there may be an overactivation of thrombin, leading to an increased risk of blood clots forming.

Protein S deficiency can be caused by several factors, including genetic mutations, vitamin K deficiency, and certain medical conditions such as liver disease or cancer. It is usually diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies.

Treatment for protein S deficiency typically involves replacing the missing protein with intravenous immune globulin (IVIG) or recombinant human protein S. In some cases, medications that inhibit thrombin activity, such as heparins or direct thrombin inhibitors, may also be used to reduce the risk of blood clots forming.

Preventing protein S deficiency involves ensuring adequate intake of vitamin K through dietary sources or supplements, managing underlying medical conditions, and avoiding factors that can increase the risk of bleeding or thrombosis, such as smoking, obesity, and inactivity.

In summary, protein S deficiency is a condition characterized by low levels of protein S, which increases the risk of developing blood clots. It can be caused by several factors and treated with replacement therapy or medications that inhibit thrombin activity. Prevention involves ensuring adequate vitamin K intake and managing underlying medical conditions.

People with factor V deficiency may experience spontaneous bleeding or bruising, especially during childhood. The symptoms can range from mild to severe and may include:

1. Easy bruising
2. Nosebleeds
3. Bleeding gums
4. Heavy menstrual periods
5. Prolonged bleeding after injuries or surgery
6. Intestinal bleeding
7. Bleeding in the joints

Factor V deficiency is caused by a genetic mutation that affects the production of factor V protein. The disorder can be inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause symptoms. In some cases, the disorder may be caused by a mutation in both copies of the gene, leading to more severe symptoms.

There is no cure for factor V deficiency, but treatment options are available to manage the symptoms. These may include:

1. Desmopressin, a medication that stimulates the release of von Willebrand factor, which helps to improve clotting.
2. Fresh frozen plasma or cryoprecipitate, which contain factors V and VIII, can be given intravenously to replace missing clotting factors.
3. Surgical intervention may be necessary in some cases, such as when bleeding is severe or persistent.
4. Lifestyle modifications, such as avoiding contact sports and taking precautions to prevent injuries, can also help manage the condition.

Early diagnosis and treatment of factor V deficiency are crucial to prevent complications and improve quality of life. If you suspect you or your child may have factor V deficiency, consult a healthcare professional for proper evaluation and management.

A condition in which spontaneous abortions occur repeatedly, often due to an underlying cause such as a uterine anomaly or infection. Also called recurrent spontaneous abortion.

Synonym(s): habitual abortion, recurrent abortion, spontaneous abortion.

Antonym(s): multiple pregnancy, retained placenta.

Example Sentence: "The patient had experienced four habitual abortions in the past year and was concerned about her ability to carry a pregnancy to term."

There are several types of coagulation protein disorders, including:

1. Hemophilia A: This is the most common type of bleeding disorder and is caused by a deficiency of factor VIII, a protein that plays a crucial role in blood clotting.
2. Hemophilia B: This is caused by a deficiency of factor IX, another important protein involved in blood clotting.
3. Von Willebrand disease: This is the most common bleeding disorder and is caused by a deficiency of von Willebrand factor, a protein that helps platelets stick together to form blood clots.
4. Platelet dysfunction: This is a rare condition where platelets do not function properly, leading to an increased risk of bleeding.
5. Protein C and protein S deficiencies: These are rare conditions caused by a deficiency of protein C and protein S, which are important proteins involved in blood clotting.

Symptoms of coagulation protein disorders can include easy bruising, frequent nosebleeds, bleeding gums, and prolonged bleeding after injury or surgery. Treatment for these disorders typically involves replacing the missing protein or modulating the body's immune system to prevent antibodies from attacking the protein. In some cases, treatment may also involve blood transfusions or medications to help regulate blood clotting.

It is important to note that coagulation protein disorders can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific disorder and the genetic mutation causing it. Genetic testing and counseling can help identify individuals at risk of inheriting these disorders and provide information on appropriate treatment and management options.

The symptoms of RVO can vary depending on the severity of the blockage, but may include:

* Blurred vision
* Double vision
* Flashes of light
* Eye pain
* Reduced peripheral vision

RVO is typically diagnosed through a comprehensive eye exam, which may include imaging tests such as fluorescein angiography or optical coherence tomography (OCT).

Treatment for RVO depends on the severity of the condition and may include:

* Medications to reduce inflammation and improve blood flow
* Injections of medication into the eye
* Laser surgery to clear blockages or reduce inflammation
* Vitrectomy, a surgical procedure to remove the vitreous gel and blood from the eye

Early diagnosis and treatment of RVO can help prevent or reduce vision loss. However, in some cases, permanent vision loss may occur despite treatment.

Preventing RVO is not always possible, but controlling risk factors such as high blood pressure, diabetes, and hypertension can help reduce the likelihood of developing the condition. Maintaining a healthy lifestyle, including regular exercise, a balanced diet, and not smoking, can also help reduce the risk of RVO.

There are several types of thrombosis, including:

1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.

The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:

1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic

Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.

Symptoms of venous thrombosis may include pain, swelling, warmth, and redness in the affected limb. In some cases, the clot can break loose and travel to the lungs, causing a potentially life-threatening condition called Pulmonary Embolism (PE).

Treatment for venous thrombosis typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.

Prevention of venous thrombosis includes encouraging movement and exercise, avoiding long periods of immobility, and wearing compression stockings or sleeves to compress the veins and improve blood flow.

Thromboembolism can be caused by a variety of factors, such as injury, surgery, cancer, and certain medical conditions like atrial fibrillation. It can also be inherited or acquired through genetic mutations.

The symptoms of thromboembolism depend on the location of the clot and the severity of the blockage. They may include:

* Swelling or redness in the affected limb
* Pain or tenderness in the affected area
* Weakness or numbness in the affected limb
* Shortness of breath or chest pain if the clot has traveled to the lungs (pulmonary embolism)
* Dizziness, lightheadedness, or fainting

Thromboembolism can be diagnosed through a variety of tests, such as ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), and blood tests. Treatment typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, thrombolysis or clot-busting drugs may be used to dissolve the clot. Filters can also be placed in the vena cava to prevent clots from traveling to the lungs.

Prevention of thromboembolism includes:

* Moving around regularly to improve blood flow
* Avoiding long periods of immobility, such as during long-distance travel
* Elevating the affected limb to reduce swelling
* Compression stockings to improve blood flow
* Avoiding smoking and managing weight
* Taking anticoagulant medications if recommended by a healthcare provider.

1. Innate immunity: This is the body's first line of defense against infection, and it involves the recognition and elimination of pathogens by cells and proteins that are present from birth.
2. Acquired immunity: This type of immunity develops over time as a result of exposure to pathogens, and it involves the production of antibodies and other immune cells that can recognize and eliminate specific pathogens.
3. Cell-mediated immunity: This is a type of immunity that involves the activation of immune cells, such as T cells and macrophages, to fight off infection.
4. Genetic resistance: Some individuals may have a genetic predisposition to disease resistance, which can be influenced by their ancestry or genetic makeup.
5. Environmental factors: Exposure to certain environmental factors, such as sunlight, clean water, and good nutrition, can also contribute to disease resistance.

Disease resistance is an important concept in the medical field, as it helps to protect against infectious diseases and can reduce the risk of illness and death. Understanding how disease resistance works can help healthcare professionals develop effective strategies for preventing and treating infections, and it can also inform public health policies and interventions aimed at reducing the burden of infectious diseases on individuals and communities.

... (APCR) is a hypercoagulability (an increased tendency of the blood to clot) characterized by a ... Sheppard DR (2000). "Activated protein C resistance: the most common risk factor for venous thromboembolism". J Am Board Fam ... APC (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. APC resistance is the inability of protein C to cleave ... Dahlbäck B (2003). "The discovery of activated protein C resistance". J. Thromb. Haemost. 1 (1): 3-9. doi:10.1046/j.1538- ...
The activated protein C resistance (APCR) test is a coagulation test used in the evaluation and diagnosis of activated protein ... The aPTT-based APC resistance test involves a modified aPTT test performed in the presence and absence of activated protein C ( ... Mueck AO (2010). "Exogenous hormones, the risk of venous thromboembolism, and activated protein C resistance". Menopause. 17 (6 ... "Laboratory assessment of Activated Protein C Resistance/Factor V-Leiden and performance characteristics of a new quantitative ...
"Sterol resistance in CHO cells traced to point mutation in SREBP cleavage-activating protein". Cell. 87 (3): 415-26. doi: ... Sterol regulatory element-binding protein cleavage-activating protein, also known as SREBP cleavage-activating protein or SCAP ... 2008). "Expression of sterol regulatory element-binding transcription factor (SREBF) 2 and SREBF cleavage-activating protein ( ... SCAP is a regulatory protein that is required for the proteolytic cleavage of the sterol regulatory element-binding protein ( ...
In cell culture, overexpression of PIAS3 demonstrated an increased resistance of HeLa cells to ionizing radiation. This ... Protein inhibitor of activated STAT (PIAS), also known as E3 SUMO-protein ligase PIAS, is a protein that regulates ... PIAS proteins act as transcriptional co-regulators with at least 60 different proteins in order to either activate or repress ... PIAS protein entry at the Protein Information Resource (PIR) PIAS+Proteins at the US National Library of Medicine Medical ...
De Stefano V, Leone G (1995). "Resistance to activated protein C due to mutated factor V as a novel cause of inherited ... Nichols WL, Heit JA (September 1996). "Activated protein C resistance and thrombosis". Mayo Clin Proc. 71 (9): 897-8. doi: ... May 1994). "Mutation in blood coagulation factor V associated with resistance to activated protein C". Nature. 369 (6475): 64-7 ... Russell viper venom-based and activated partial thromboplastin time-based screening assays for resistance to activated protein ...
Activated protein C resistance occurs when APC is unable to perform its functions. This disease has similar symptoms to protein ... Activated protein C-protein C inhibitor ^ α: GLA-domainless protein C is produced by selective proteolysis between residues 82 ... Walker FJ (June 1980). "Regulation of activated protein C by a new protein. A possible function for bovine protein S". The ... 4673 The protein C zymogen is activated when it binds to thrombin, another protein heavily involved in coagulation, and protein ...
"Mali acroangiodermatitis in homozygous activated protein C resistance". Arch Dermatol. 141 (3): 396-7. doi:10.1001/archderm. ...
Mitogen-activated protein kinase 4 is an enzyme that in humans is encoded by the MAPK4 gene. Mitogen-activated protein kinase 4 ... December 2000). "Arabidopsis map kinase 4 negatively regulates systemic acquired resistance". Cell. 103 (7): 1111-20. doi: ... Tyrosine kinase growth factor receptors activate mitogen-activated protein kinases which then translocate into the nucleus ... Li L, Wysk M, Gonzalez FA, Davis RJ (February 1994). "Genomic loci of human mitogen-activated protein kinases". Oncogene. 9 (2 ...
They are induced as part of systemic acquired resistance. Infections activate genes that produce PR proteins. Some of these ... Many proteins found in wine are grape pathogen-related proteins. Those include thaumatin-like proteins and chitinases. Many ... unrelated resistance proteins Loon LC (1985). "Pathogenesis-related proteins". Plant Molecular Biology. 4 (2-3): 111-116. doi: ... Salicylic acid plays a role in the resistance to pathogens by inducing the production of pathogenesis-related proteins. ...
He determined that activated protein C (APC) resistance is the most common inherited risk factor of venous thrombosis. Dahlbäck ... Zöller, B.; Dahlbäck, B. (1994). "Linkage between inherited resistance to activated protein C and factor V gene mutation in ... Svensson, Peter J.; Dahlback, Bjorn (1994). "Resistance to Activated Protein C as a Basis for Venous Thrombosis". New England ... Dahlback, B.; Hildebrand, B. (1994). "Inherited resistance to activated protein C is corrected by anticoagulant cofactor ...
... involvement in insulin resistance via Akt, serine/arginine-rich protein 40, and ... Ceramide-activated protein phosphatases (CAPPs) are a group of enzymes that are activated by the lipid second messenger ... Long chain ceramides activate protein phosphatase-1 and protein phosphatase-2A. Activation is stereospecific and regulated by ... Wolff, R., Dobrowsky, R., Bielawska, A., Obeid, L., & Hannun, Y. (1994). Role of ceramide-activated protein phosphatase in ...
By activating a phosphatase, LAM can inhibit LPS and IFN-γ induced protein tyrosine phosphorylation in monocytes. This ... IL-12 is important for innate resistance to M. tuberculosis infections. It activates natural killer cells which produce IFN-γ ... of Mycobacterium tuberculosis promotes protein tyrosine dephosphorylation and inhibition of mitogen-activated protein kinase in ... ManLAM is able to activate the serine/threonine kinase Akt via phosphorylation which is then able to phosphorylate Bad. ...
July 2003). "Rnd proteins function as RhoA antagonists by activating p190 RhoGAP". Current Biology. 13 (13): 1106-15. doi: ... the issue of drug resistance remains. Minimizing or postponing this resistance would the necessary dose to eradicate the tumor ... July 2003). "p250GAP, a novel brain-enriched GTPase-activating protein for Rho family GTPases, is involved in the N-methyl-d- ... RhoA proteins help potentiate the transcription independent of ternary complex factors when activated while simultaneously ...
An elevated level of ceramide can cause insulin resistance by inhibiting the ability of insulin to activate the insulin signal ... Ceramides cause endothelial dysfunction by activating protein phosphatase 2 (PP2A). In mitochondria, ceramide suppresses the ... "Ceramide-activated phosphatase mediates fatty acid-induced endothelial VEGF resistance and impaired angiogenesis". The American ... Ceramides induce insulin resistance in many tissues by inhibition of Akt/PKB signaling. Aggregation of LDL cholesterol by ...
Activated protein C resistance that is not attributable to factor V mutations is probably caused by other factors and remains a ... of people with protein C deficiency and about a third of those with protein S deficiency. People with activated protein C ... Many studies had previously indicated that many people with thrombosis showed resistance activated protein C. In 1994 a group ... May 1994). "Mutation in blood coagulation factor V associated with resistance to activated protein C". Nature. 369 (6475): 64-7 ...
... and to assess activated protein C resistance (APCR). The CAT ETP-based APC resistance test is especially sensitive to estrogen- ... "Interlaboratory variability of activated protein C resistance using the ETP-based APC resistance assay". Res Pract Thromb ... "Validation and standardization of the ETP-based activated protein C resistance test for the clinical investigation of steroid ... "Proof of concept of a new scale for the harmonization and the standardization of the ETP-based APC resistance". J Thromb ...
... is a substrate of CYP3A4 and multidrug resistance-associated protein 2; drugs that inhibit these enzymes will ... increase the half-life of cabozantinib and potentially increase its adverse effects; drugs that activate them may cause ... It inhibits the following receptor tyrosine kinases: MET (hepatocyte growth factor receptor protein) and VEGFR, RET, GAS6 ... blood or protein in urine, wounds that don't heal well, and facial swelling. Grapefruit and grapefruit juice should be avoided ...
Rosendorff A, Dorfman DM (June 2007). "Activated protein C resistance and factor V Leiden: a review". Arch. Pathol. Lab. Med. ... Factor Va is inactivated following cleavage by activated protein C. Activated protein C cleaves Factor Va in both its light and ... if Factor V is cleaved by activated protein C instead of thrombin, it can serve as a cofactor for activated protein C. Once ... Contributions of protein-protein and protein-membrane interactions toward complex formation". J. Biol. Chem. 265 (7): 3708-18. ...
... where sterol regulatory element-binding protein 1 (SREBP-1c) is the major transcription factor). ChREBP is normally activated ... By contrast, high blood levels of insulin, due to a high carbohydrate meal or insulin resistance, strongly induces SREBP-1c ... But in conditions of obesity, insulin resistance, or type 2 diabetes de novo lipogenesis is reduced in adipose tissue (where ... Fructose consumption (in contrast to glucose) activates both SREBP-1c and ChREBP in an insulin independent manner. Although ...
IL-6 activates the CCAAT enhancer-binding protein transcription factors which activate MDR1 gene expression (see Alteration of ... Antineoplastic resistance, often used interchangeably with chemotherapy resistance, is the resistance of neoplastic (cancerous ... MDR1 is activated through NF-κB, a protein complex which acts as a transcription factor. In the rat, an NF-κB binding site is ... MDR proteins are known to be drug-resistance genes, and are highly expressed in various cancers. Inhibition of the MDR genes ...
It is a member of the signaling protein mitogen-activated protein kinase (MAPK) kinase kinase. EIN2 is required for ethylene ... natural resistance-associated macrophage protein) family of metal transporters; it comprises a large, N-terminal portion ... Copper ion is supplied by a transmembrane protein responsive-to-antagonist 1 (RAN1) from antioxidant protein 1 (ATX1) via ... of which the C-terminal portion of the protein can activate different transcription factors to bring about the effects of ...
... indirectly activate SIRT1 by activation of AMP-activated protein kinase (AMPK), which increases NAD+ levels (which is the ... This has been linked to insulin resistance in the obese. Human Sirt1 has been reported having 136 direct interactions in ... SIRT1 mediated HR requires the WRN protein. WRN protein functions in double-strand break repair by HR. WRN protein is a RecQ ... Metformin activates both PRKA and SIRT1. Although neither resveratrol or SRT1720 directly activate SIRT1, resveratrol, and ...
Insulin activates mTORC1 and causes dissociation of TSC from the surface of lysosomes. Resistance to ischemia-reperfusion ... "The TSC complex is required for the benefits of dietary protein restriction on stress resistance in vivo". Cell Reports. 8 (4 ... injury by protein restriction is mediated by activation of the tuberous sclerosis complex. Dibble CC, Elis W, Menon S, Qin W, ...
... activating mutations in PIK3CA (PI3K), activating mutations in the proto-oncogene tyrosine-protein kinase Src, etc.) that lead ... March 2003). "Role of the estrogen receptor coactivator AIB1 (SRC-3) and HER-2/neu in tamoxifen resistance in breast cancer". ... The nuclear receptor coactivator 3 also known as NCOA3 is a protein that, in humans, is encoded by the NCOA3 gene. NCOA3 is ... The ratio of PAX2 to AIB-1 protein expression may be predictive of the effectiveness of tamoxifen in breast cancer treatment. ...
... both proteins activate expression. The difference relates to their respective response to tetracycline or doxycycline (Dox, a ... Tetracycline-controlled gene expression is based upon the mechanism of resistance to tetracycline antibiotic treatment found in ... The Tet-Off system makes use of the tetracycline transactivator (tTA) protein, which is created by fusing one protein, TetR ( ... The resulting tTA protein is able to bind to DNA at specific TetO operator sequences. In most Tet-Off systems, several repeats ...
Insulin resistance syndromes may be divided into type A (HAIR-AN) and type B syndromes.: 978 The majority of cases of ... This activates the insulin-like growth factor receptors, which leads to proliferation of keratinocytes, fibroblasts and other ... Acanthosis nigricans is caused by increased activation of growth factor receptor proteins, usually due to endocrine dysfunction ... This activates keratinocyte IGF receptors, particularly IGF-1. At high concentrations, insulin may also displace IGF-1 from ...
"Evidence that pp42, a major tyrosine kinase target protein, is a mitogen-activated serine/threonine protein kinase". www.pnas. ... His PubMed publication listing includes a posthumous publication on the development of tumor drug resistance. Obituary at ... He was a co-discoverer of Mitogen-activated protein kinase, publishing a widely cited paper on the topic in 1989. He also ... "Microenvironmental agonists generate de novo phenotypic resistance to combined ibrutinib plus venetoclax in CLL and MCL". Blood ...
"Sterol resistance in CHO cells traced to point mutation in SREBP cleavage-activating protein". Cell. 87 (3): 415-26. doi: ... Nov 1984). "The human LDL receptor: a cysteine-rich protein with multiple Alu sequences in its mRNA". Cell. 39 (1): 27-38. doi: ... Reiss Y, Goldstein JL, Seabra MC, Casey PJ, Brown MS (Jul 1990). "Inhibition of purified p21ras farnesyl:protein transferase by ... Oct 1993). "SREBP-1, a basic-helix-loop-helix-leucine zipper protein that controls transcription of the low density lipoprotein ...
Active GTP-bound G12 alpha subunit interacts with and activates ARHGEF1, ARHGEF11, and ARHGEF12. These ARHGEF proteins function ... Wang L, Guo D, Xing B, Zhang JJ, Shu HB, Guo L, Huang XY (September 2011). "Resistance to inhibitors of cholinesterase-8A (Ric- ... these two proteins comprise one of the four classes of heterotrimeric G protein alpha subunits. Heterotrimeric G proteins ... Guanine nucleotide-binding protein subunit alpha-12 is a protein that in humans is encoded by the GNA12 gene. The GNA12 gene ...
This binding is dependent on binding to a protein called Hfq. Transcription of the GcvB RNA is activated by the adjacent GcvA ... It has been shown by gene deletion that GcvB is a regulator of acid resistance in E. coli. GcvB enhances the ability of the ... Jin Y, Watt RM, Danchin A, Huang JD (2009). "Small noncoding RNA GcvB is a novel regulator of acid resistance in Escherichia ... Pulvermacher SC, Stauffer LT, Stauffer GV (January 2009). "Role of the Escherichia coli Hfq protein in GcvB regulation of oppA ...
Class 2 systems use a single large Cas protein for the same purpose. Class 1 is divided into types I, III, and IV; class 2 is ... Martz, Lauren (August 31, 2017). "Cutting through resistance". Biocentury. Retrieved July 18, 2020. Maurer, Allan (November 19 ... "Structures of CRISPR Cas3 offer mechanistic insights into Cascade-activated DNA unwinding and degradation". Nature Structural ... Class 1 systems use a complex of multiple Cas proteins to degrade foreign nucleic acids. ...
Type I IFNs further activate p38 mitogen-activated protein kinase (MAP kinase) to induce gene transcription. Antiviral and ... The H5N1 influenza virus, also known as bird flu, has resistance to interferon and other anti-viral cytokines that is ... For instance, both type I and type II IFNs activate a member of the CRK family of adaptor proteins called CRKL, a nuclear ... PI3K activates P70-S6 Kinase 1, an enzyme that increases protein synthesis and cell proliferation; phosphorylates ribosomal ...
"The HIV-1 vpr protein induces anoikis-resistance by modulating cell adhesion process and microfilament system assembly". Cell ... "Identification and characterization of a novel activated RhoB binding protein containing a PDZ domain whose expression is ... Identification of a non-cytosolic GDI protein interacting with the small GTP-binding proteins RhoB and RhoG". The Journal of ... Identification of a non-cytosolic GDI protein interacting with the small GTP-binding proteins RhoB and RhoG". The Journal of ...
... the TrfA protein, binds to and activates oriV. In Escherichia coli, replication proceeds unidirectionally from oriV after ... The resistance genes confer resistance to the antibiotics kanamycin, ampicillin and tetracycline. In addition, RK2 contains a ... and two antibiotic resistance genes, bla and cat, which confer resistance to Ampicillin and Chloramphenicol, respectively. ... PFF1 consists of an origin of replication, oriV, an origin of transfer, oriT, a gene coding for plasmid replication proteins, ...
"Functional interaction between c-Abl and the p21-activated protein kinase gamma-PAK". Proc. Natl. Acad. Sci. U.S.A. 97 (26): ... "Overriding imatinib resistance with a novel ABL kinase inhibitor". Science. 305 (5682): 399-401. Bibcode:2004Sci...305..399S. ... Tyrosine-protein kinase ABL1 also known as ABL1 is a protein that, in humans, is encoded by the ABL1 gene (previous symbol ABL ... Welch PJ, Wang JY (November 1993). "A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl ...
In some cases the membrane permeabilization effects of viroporins activate the inflammasome, a protein complex associated with ... for its use in children or elderly people and the US CDC does not recommend drugs of this class due to widespread resistance ... which can modulate protein trafficking of viral proteins or protect the proteins from the low pH they would otherwise encounter ... The human papillomavirus 16 E5 protein, the least well-studied of the three known oncogenic HPV proteins, was reported in 2012 ...
Phosphorylation of the transcription factor may activate it and that activated transcription factor may then activate the ... A connector protein dimer (e.g. CTCF or YY1) stabilizes the loop by anchoring one member on the enhancer and the other on the ... Chen HY, Shao CJ, Chen FR, Kwan AL, Chen ZP (April 2010). "Role of ERCC1 promoter hypermethylation in drug resistance to ... An activated enhancer begins transcription of its RNA before activating a promoter to initiate transcription of messenger RNA ...
The downstream signals through ouabain-triggered protein phosphorylation events include activation of the mitogen-activated ... Zylbertal A, Kahan A, Ben-Shaul Y, Yarom Y, Wagner S (December 2015). "Prolonged Intracellular Na+ Dynamics Govern Electrical ... Protein-protein interactions play a very important role in Na⁺-K⁺ pump-mediated signal transduction. For example, the Na⁺-K⁺ ... this membrane protein can also relay extracellular ouabain-binding signalling into the cell through regulation of protein ...
But MyD88 also activates mitogen‐activated protein kinases (MAPKs). However, several strains of lactic acid bacteria have been ... On the other hand, a protective SNP also exists - S249P is possibly liked to protection from bronchial asthma and resistance ... Toll-like receptor 6 is a protein that in humans is encoded by the TLR6 gene. TLR6 is a transmembrane protein, member of toll- ... It is also known that TLR2/6 binds some viral products, among them hepatitis C core and NS3 protein from the hepatitis C virus ...
... subunit of voltage-activated Ca2+ channels are associated with insulin resistance and type 2 diabetes in Pima Indians". ... CACNA1E+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH) R-Type+Calcium+Channel at the US ... "Structure and functional expression of a member of the low voltage-activated calcium channel family". Science. 260 (5111): 1133 ...
A lack of sleep also causes increases in the creation of proteins in the body that cause chronic pain by reducing the body's ... Insulin resistance occurs when cells fail to use insulin efficiently which results in high blood sugar. Furthermore, when ... affect glucose levels since the fight-or-flight response causes increased hormone levels as one's nerve cells become activated ... When the body is going through heavy sleep loss, it can form insulin resistance which is a precursor to diabetes. ...
To develop, the larvae must be fed both nectar for carbohydrates and pollen for protein. Bumblebees feed nectar to the larvae ... they had applied the equations of air resistance to insects and found their flight was impossible, but "One shouldn't be ... The chill-coma temperature in relation to flying insects is the temperature at which flight muscles cannot be activated. ...
Many cancers make proteins such as PD-L1 that also bind to the PD-1 receptor, thus shutting down the ability of the body to ... Normally, the PD-1 receptor on activated T-cells binds to the PD-L1 or PD-L2 ligands present on normal cells in the body, ... Syn, Nicholas L; Teng, Michele W L; Mok, Tony S K; Soo, Ross A (2017). "De-novo and acquired resistance to immune checkpoint ... It works by targeting the cellular pathway of proteins found on the body's immune cells and some cancer cells, known as PD-1/PD ...
CDKs perform a common biochemical reaction called phosphorylation that activates or inactivates target proteins to orchestrate ... For cells with a longer cell cycle time and a significantly long G1 phase, there is a second peak of resistance late in G1. The ... p21 is activated by p53 (which, in turn, is triggered by DNA damage e.g. due to radiation). p27 is activated by Transforming ... Two families of genes, the cip/kip (CDK interacting protein/Kinase inhibitory protein) family and the INK4a/ARF (Inhibitor of ...
Moreover, many of the open reading frames (ORFs) on CII seem to code for proteins of unknown function. When genes of unknown ... One of the 1O2 induced sRNAs SorY (1O2 resistance RNA Y) was shown to be induced under several stress conditions and conferred ... For example, decrease in oxygen tensions activates the synthesis of photosynthetic machinery (including photosystems, antenna ... It also has an impact on resistance against organic hydroperoxides. A cluster of four homologous sRNAs called CcsR for ...
J Exp Med 145: 1-9. Rao A, Ko WW, Faas SJ, Cantor H. Binding of antigen in the absence of histocompatibility proteins by ... Nature Immunology, 2004;5:516 Lu L, Ikizawa K, Hu D, Werneck MBF, Wucherpfennig KW, Cantor H. Regulation of activated CD4+ T ... Avery AC, Zhao ZS, Rodriquez A, Bikoff EK, Soheilian M, Foster CS, Cantor H.. Resistance to herpes stromal keratitis conferred ... Definition of a novel T-cell dependent response associated with genetic resistance to bacterial infection. J Exp Med 170:145- ...
... which in turn activates an electrical generator." Semiconductors David O. Ramos of Isabela, and Martin Bresciani of Guaynabo, ... Well-known examples of polymers include plastics, DNA and proteins. According to the abstract released by the U.S. Patent & ... Lissette Martinez is an electrical engineer and rocket scientist. Martinez is the lead electrical engineer for the Space ... He received a BS degree in electrical engineering (magna cum laude) from the University of Puerto Rico - Mayagüez, and an MS ...
They do this by aiding complement resistance. The stalk protein domain is also alternatively named the internal passenger ... This may be due to BadA's inducing the transcription of proangiogenic factors, as it activates of NF-κB as well as hypoxia- ... Protein pages needing a picture, Protein families, Protein domains, Virulence factors, Gram-negative bacteria, Secretion, ... First, biogenesis of proteins in the Type V Secretion System (T5SS). Second, it is thought to target the protein to the inner ...
The protein was detected in and purified from cultures of Phytohaemagglutinin-activated human T-cell leukemia SKW-3 cells. ... In support of this notion, Gemigliptin, an anti-diabetic drug, has been shown reduce insulin resistance and concurrently ... The secreted protein consists of 133`amino acids (mouse Lect2 consists of two varieties a typical 151 amino acid protein and an ... LECT2 protein is widely expressed in vascular tissues, smooth muscle cells, adipocytes, cerebral neurons, apical squamous ...
Long chain FA are first activated via esterification with coenzyme A to produce a fatty acid-coA complex which can then cross ... This complex is then transported through the inner mitochondrial membrane via a transporter protein called carnitine- ... which has been implicated in the development of insulin resistance. Because of its inhibitory effects on L-carnitine ... This is done by adapting myocardial cells to lower fatty acid inflow and by activating glycolysis; the heart eventually begins ...
The HIF stabilizer activates the activity of EPO due to anemia induced hypoxia, metabolic stress, and vasculogenesis-the ... A common feature of all HBOCs is their resistance to dissociate when dissolved in media, which contrasts hemoglobin of natural ... Like most transcription factors, the HIF transcription factor is responsible for the expression of a protein. ... degradation is prevented and genes encoding EPO can then be activated. The mechanism for this Co2+ N terminus stabilization is ...
Probiotics stimulate production of a protein that maintains the strength of the intestinal barrier and have beneficial effects ... additionally antibiotic resistance is a growing problem. Replacing typical antibiotic treatments with novel FMT treatment ... as studies have shown that bacteria in the gut can activate stress response through the vagus nerve, a cranial nerve ...
... these proteins activate two important transcription factors: NF-κB is a dimeric protein responsible for expression of various ... However, available evidence suggests that MYD88 is dispensable for human resistance to common viral infections and to all but a ... The MyD88 protein acts as an adapter, connecting proteins that receive signals from outside the cell to the proteins that relay ... Another adaptor protein, which is activated by TLR3 and TLR4, is called TIR domain-containing adapter-inducing IFN-β (TRIF). ...
2016 Protein engineered systems for delivery of molecules 2016 Fluorinated protein-based polymeric carriers 2017 Protein ... She develops stable, activate fluorinated phosphotriesterase (PTE) variants by combining PTE with non-canonical amino acids. ... blow to cancer cells by delivering both a chemotherapeutic agent and RNA interfering technology that silences drug resistance ... retrieved 2019-02-17 Fluorinated protein-based polymeric carriers, retrieved 2019-02-17 Protein nanofibers from self-assembling ...
The activated GR complex up-regulates the expression of anti-inflammatory proteins in the nucleus or represses the expression ... The GR is abnormal in familial glucocorticoid resistance. In central nervous system structures, the glucocorticoid receptor is ... the heat shock protein 70 (hsp70) and the protein FKBP4 (FK506-binding protein 4). The endogenous glucocorticoid hormone ... Hulkko SM, Wakui H, Zilliacus J (August 2000). "The pro-apoptotic protein death-associated protein 3 (DAP3) interacts with the ...
During the Axis occupation of Greece Zervas played an active part in the Greek Resistance as a member of EDES; he was impisoned ... The ability of Z-protection to prevent racemization of activated derivatives of the protected amino acids and the importance ... The insulin peptide hormone features two protein chains cross-linked by disulfide bridges from cysteine thiols. For this reason ...
"Entrez Gene: PRKDC protein kinase, DNA-activated, catalytic polypeptide". Meek K, Dang V, Lees-Miller SP (2008). DNA-PK: the ... "Up-regulation of DNA-dependent protein kinase correlates with radiation resistance in oral squamous cell carcinoma". Cancer Sci ... Gell D, Jackson SP (September 1999). "Mapping of protein-protein interactions within the DNA-dependent protein kinase complex ... The DNA-Pkcs protein is a serine/threonine protein kinase comprising a single polypeptide chain of 4,128 amino acids. DNA-PKcs ...
Blood tests show the level of IgM in the blood and the presence of proteins, or tumor markers, that are the key signs of ... Prothrombin time, activated partial thromboplastin time, thrombin time, and fibrinogen tests should be performed. Platelet ... When primary or secondary resistance invariably develops, salvage therapy is considered. Allogeneic stem cell transplantation ... Serum protein electrophoresis results indicate evidence of a monoclonal spike but cannot establish the spike as IgM. An M ...
The activation of these receptors by acetylcholine will activate an intracellular G protein, that in turn will activate the ... The muscle contraction will cause the diameter of the bronchus to decrease, therefore increasing its resistance to airflow. ... TH2-type lymphocytes are activated, with an increase in T cells expressing CD25 (IL-2R), and B cells expressing CD 23, causing ... decrease airway resistance, and increase delivery of air to the alveoli during respiration. Unlike the SABAs, these medications ...
Xu SN, Wang TS, Li X, Wang YP (September 2016). "SIRT2 activates G6PD to enhance NADPH production and promote leukaemia cell ... Glucose-6-phosphate dehydrogenase deficiency Genetic resistance to malaria Thomas D, Cherest H, Surdin-Kerjan Y (March 1991). " ... Protein Science. 17 (8): 1403-11. doi:10.1110/ps.035352.108. PMC 2492815. PMID 18493020. Eger-Neufeldt I, Teinzer A, Weiss L, ... Moreover, G6PD is one of a number of glycolytic enzymes activated by the transcription factor hypoxia-inducible factor 1 (HIF1 ...
Phenprocoumon-induced hepatitis delaying precise diagnosis in a thrombophilic patient with activated protein C resistance due ... Resistance to activated protein C due to factor V R506Q mutation as a cause of venous thrombosis. Dahlbäck B. Dahlbäck B. Rev ... Phenprocoumon-induced hepatitis delaying precise diagnosis in a thrombophilic patient with activated protein C resistance due ... Phenprocoumon-induced hepatitis delaying precise diagnosis in a thrombophilic patient with activated protein C resistance due ...
Acquired Activated Protein C Resistance, Thrombophilia and Adverse Pregnancy Outcomes: A Study Performed in an Irish Cohort of ... The most significant common inherited risk factor for thrombophilia is activated protein C resistance (APCR), a poor ... Acquired Activated Protein C Resistance, Thrombophilia and Adverse Pregnancy Outcomes: A Study Performed in an Irish Cohort of ... Changes in the levels of coagulation factors: FV, FVIII, and FIX, and anticoagulant factors: protein S (PS) and protein C (PC) ...
Activated protein C resistance (checks for the Factor V Leiden mutation). *Antithrombin III levels ...
Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Factor V Leiden mutation is ... Endogenous plasma activated protein C levels and the effect of enoxaparin and drotrecogin alfa (activated) on markers of ... Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. Deficiency of these ... protein C, or protein S deficiency. [16] In 1997, Nuss et al reported that 70% of children with a diagnosis of pulmonary ...
Hereditary resistance to activated protein C, see Factor V Leiden thrombophilia. *Hereditary retinal aplasia, see Leber ... Hereditary thrombophilia due to protein C deficiency, see Protein C deficiency. *Hereditary thrombophilia due to protein S ... Hypobetalipoproteinemia with accumulation of apolipoprotein B-like protein in intestinal cells, see Chylomicron retention ...
... myxovirus resistance gene; OAS, oligoadenylate synthetase; PKR, protein kinase RNA-activated; ISG15, interferon-stimulated gene ... An overview of protein-protein interaction network of a set of proteins, identified in rainbow trout proteome profiling, ... The set of genes/proteins identified were ARP1 actin-related protein 1 homolog B (ACTR1B), adaptor-related protein complex 1 ... protein kinase RNA-activated (PKR), viperin, interferon-stimulated gene 15 (ISG15), IFN-induced protein with tetratricopeptide ...
Activated Protein C Resistance. EN. dc.subject. Factor V. EN. dc.subject. Infarction. EN. ...
PCBs activate AHR proteins to alter gene expression and cell function.. Hahn and colleagues found that killifish have ... Identified genes involved in contaminant resistance.. *Discovered genes in AHR pathways that likely play a role in resistance. ... With the AHR pathway turned off, PCBs can no longer activate the protein to alter the gene expression and function of cells ... Discovered killifish resistance to pollutants is at least partly genetic.. *Analyzed how adapting to contaminants leaves ...
Resistance to activated protein C caused by the R506Q mutation in the gene for factor V is a common risk factor for venous ... Resistance to activated protein C due to mutated factor V as a novel cause of inherited thrombophilia.. De Stefano V; Leone G. ... Activated protein C resistance--a major risk factor for thrombosis.. Rosén SB; Sturk A. Eur J Clin Chem Clin Biochem; 1997 Jul ... 8. Resistance to activated protein C in women using oral contraceptives.. Spannagl M; Dick A; Assmann A; Heinemann L; Schramm W ...
FAAH is a protein that breaks down anandamide, also known as the "bliss molecule," which is a neurotransmitter that binds to ... These are some of the same receptors that are activated by marijuana. With less FAAH activity, this patient was found to have ... more circulating levels of anandamide, which may explain her resistance to feeling pain. ...
In addition, protein S levels decrease during pregnancy, [7] and increased resistance to activated protein C is observed in the ... Increased resistance to activated protein C: Observed in the second and third trimesters of pregnancy ... Postpartum: Prophylaxis with prophylactic- or intermediate-dose LMWH or, in women with no protein C or S deficiency, vitamin K ... Postpartum: Prophylaxis with prophylactic- or intermediate-dose LMWH or, in women with no protein C or S deficiency, vitamin K ...
Bennet L, Odeberg H. Resistance to activated protein C, highly prevalent amongst users of oral contraceptives with venous ... Known thrombogenic mutations (e.g., factor V Leiden; prothrombin mutation; and protein S, protein C, and antithrombin ... Thrombotic risk of women with hereditary antithrombin III-, protein C- and protein S-deficiency taking oral contraceptive ... Effects of oral contraception on liver function tests and serum proteins in women with active schistosomiasis. Contraception ...
... and clotting protein, were higher in the group of ME.25 and ME5.0 than in the control and ME1.25 at several time points. Growth ... This study investigated the effect of a moringa water extract on the immune response, resistance against V. alginolyticus, and ... Phagocytosis is stimulated by the components of the putative ProPO-activating system. PO is a sticky protein that attaches to ... glucan binding protein, and recognition molecules), and a multimeric system (clotting protein cascade, prophenoloxidase system ...
DNA-Activated Protein Kinase/antagonists & inhibitors; Drug Resistance, Neoplasm; Enzyme Inhibitors/pharmacology; High- ... Double-strand break repair capacity is recognized as an important mechanism in drug resistance and is therefore a potential ...
o Protease-Activated Receptors A group of cell surface G-protein coupled receptors that are involved in the proteolytic ... Studies on the role of leukocytes in thrombosis and the contribution of markers of inflammation to thrombolytic resistance are ... There are a number of proteins - antithrombin, protein C, protein S, clotting factor V, prothrombin, thrombomodulin, ... Thrombin may also activate endothelial cells through PAR(s) and regulate the adhesive protein expression on the surface. ...
Thrombophilia due to activated protein C resistance MedGen: C1861171 OMIM: 188055 GeneReviews: Factor V Leiden Thrombophilia ... The activated protein is a cofactor that participates with activated coagulation factor X to activate prothrombin to thrombin. ... General protein information Go to the top of the page Help Preferred Names. coagulation factor V. Names. activated protein c ... which is known as activated protein C resistance. [provided by RefSeq, Oct 2008]. Expression. Biased expression in liver (RPKM ...
The RIT1 gene provides instructions for making a protein that helps cells survive during periods of cellular stress, such as ... A rit GTPase-p38 mitogen-activated protein kinase survival pathway confers resistance to cellular stress. Mol Cell Biol. 2011 ... The RIT1 protein is turned off (inactivated) when it converts the GTP to GDP. When the protein is bound to GDP, it does not ... The RIT1 gene mutations associated with Noonan syndrome change single protein building blocks (amino acids) in the RIT1 protein ...
The patients activated protein C resistance was 1.8 (reference range , 2.1). She had an identical twin sister who had the same ... Dahlback B. Resistance to activated protein C caused by the factor VR506Q mutation is a common risk factor for venous ... Resistance to activated protein C as a basis for venous thrombo‑embolism associated with pregnancy and oral contraceptives. ... Dahlbäck B. Inherited thrombophilia: resistance to activated protein C as a pathogenic factor of venous thromboembolism. Blood ...
aPTT-based Activated Protein C Resistance (APC-R). Activated clotting time (ACT). Bethesda assays (bovine chromogenic) for ... aPTT-based Activated Protein C Resistance (APC-R), and Bethesda assays (clotting-based) for factor VIII (FVIII) inhibitor ... HEMLIBRA bridges activated factor IX and factor X to restore the function of missing activated factor VIII that is needed for ... HEMLIBRA affects intrinsic pathway clotting-based laboratory tests, including activated clotting time (ACT), activated partial ...
... that are mitochondrial derived proteins (MDP). The aim of this study was to determine MDP in normal, prediabetes and diabetes ... that are mitochondrial derived proteins (MDP). The aim of this study was to determine MDP in normal, prediabetes and diabetes ... Humanin skeletal muscle protein levels increase after resistance training in men with impaired glucose metabolism. Physiol Rep. ... AMP-activated protein kinase (AMPK) activation and mitochondrial metabolism. (24). The mitochondrial derived peptides (MDP) ...
Binding of IRS proteins to calmodulin is enhanced in insulin resistance. Biochemistry 2000; 39:5089-5096. ... IQGAP1 is a scaffold for mitogen-activated protein kinase signalling. Mol Cell Biol 2005; 25:7940-52. ... Absence of IQGAP1 protein leads to insulin resistance. J Biol Chem 2017; 292:3273-3289. ... Dephosphorylation of the nuclear factor of activated T cells (NFAT) transcription factor is regulated by an RNA-protein ...
The Ras GTPase-activating-like protein IQGAP1 mediates Nrf2 protein activation via the mitogen-activated protein kinase/ ... Binding of IRS proteins to calmodulin is enhanced in insulin resistance. Biochemistry 2000; 39:5089-5096. ... Absence of IQGAP1 protein leads to insulin resistance. J Biol Chem 2017; 292:3273-3289. ... Absence of IQGAP1 protein leads to insulin resistance. J Biol Chem 2017; 292:3273-3289. ...
Matrix metalloprotease 9 is of particular interest because it was demonstrated to be upregulated in activated monocytes and ... instead of the endosome may simultaneously explain the ability of FIPV to infect macrophages and the macrophage resistance of ... The coronavirus spike protein is a class I fusion protein, which typically requires activation by cellular proteases. Mutation ... de Haan CAM, Haijema BJ, Schellen P, Schreur PW, te Lintelo E, Vennema H, Cleavage of group 1 coronavirus spike proteins: how ...
M. Costa and R. L. Medcalf, "Differential binding of cAMP-responsive-element(CRE)-binding protein-1 and activating ... Thrombolytic therapy with t-PA at present is limited by the relatively high incidence of reocclusion and resistance to ... O. H. Lowry, N. J. Rosebrough, A. L. Farr, and R. J. Randall, "Protein measurement with the folin phenol reagent," The Journal ... Thrombolytic agents (enzyme/protein) are classified into two types based on the working mechanisms. Tissue plasminogen ...
PD-L1 protein binds to T cell B7-1/CD80 and PD-1. It suppresses T cell activation and proliferation and induces the apoptosis ... In cancer, PD-L1 provides resistance to T cell mediated lysis, enhances EMT, and enhances the tumorigenic function of Th22 ... PD-L1 is expressed on inflammatory-activated immune cells including macrophages, T cells, and B cells, keratinocytes, ... Many tumors overexpress PD-L1 protein making the PD-1:PD-L1 interaction central to several successful cancer immunotherapy ...
  • Hispidin suppressed insulin receptor substrate‑1 Ser307 phosphorylation, and significantly promoted the activation of phosphatidylinositol‑3‑kinase and Akt, via inhibition of protein kinase C theta. (spandidos-publications.com)
  • Furthermore, hispidin treatment of C2C12 muscle cells increased glucose uptake via activation of adenosine monophosphate‑activated protein kinase. (spandidos-publications.com)
  • AMP-activated protein kinase (AMPK) is a sensor of cellular energy status that plays a central role in skeletal muscle metabolism. (wellnessresources.com)
  • For the study, the researchers investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. (medindia.net)
  • The molecular reason you must restrict calories is that there is a very intricate relationship between excess fat stores and metabolism mediated by the master regulator of metabolism known as AMP-activated protein kinase (AMPK). (drsears.com)
  • The most significant common inherited risk factor for thrombophilia is activated protein C resistance (APCR), a poor anticoagulant response of APC in haemostasis, which is mainly caused by an inherited single-nucleotide polymorphism (SNP), factor V G1691A (FV Leiden) (FVL), referred as inherited APCR. (nuigalway.ie)
  • A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). (nih.gov)
  • Changes in the levels of coagulation factors: FV, FVIII, and FIX, and anticoagulant factors: protein S (PS) and protein C (PC) can alter APC function causing acquired APCR. (nuigalway.ie)
  • 18. Mutation in blood coagulation factor V associated with resistance to activated protein C. (nih.gov)
  • The activated protein is a cofactor that participates with activated coagulation factor X to activate prothrombin to thrombin. (nih.gov)
  • Laboratory Coagulation Test Interference: HEMLIBRA interferes with activated clotting time (ACT), activated partial thromboplastin time (aPTT), and coagulation laboratory tests based on aPTT, including one-stage aPTT-based single-factor assays, aPTT-based Activated Protein C Resistance (APC-R), and Bethesda assays (clotting-based) for factor VIII (FVIII) inhibitor titers. (nih.gov)
  • The F5 gene provides instructions for making a protein called coagulation factor V. This protein plays a critical role in the coagulation system, which is a series of chemical reactions that forms blood clots in response to injury. (studyquestions.org)
  • Activated protein C is involved in the delicate balance of procoagulant and anticoagulant forces of the coagulation cascade. (studyquestions.org)
  • Activated protein C inhibits coagulation through the inactivation of membrane-bound activated factor V and activated factor VIII. (studyquestions.org)
  • APC resistance--most frequent familial thrombophilia]. (nih.gov)
  • 16. Resistance to activated protein C due to mutated factor V as a novel cause of inherited thrombophilia. (nih.gov)
  • Defects in this gene result in either an autosomal recessive hemorrhagic diathesis or an autosomal dominant form of thrombophilia, which is known as activated protein C resistance. (nih.gov)
  • Is Thrombophilia the same as protein C deficiency? (studyquestions.org)
  • Is protein S deficiency a thrombophilia? (studyquestions.org)
  • Mild protein S deficiency is a hereditary type of thrombophilia or clotting disorder, and is more common than the severe form of the disorder. (studyquestions.org)
  • Factor V Leiden mutation, Protein C and S deficiency are the leading causes of thrombophilia with strong association of Factor V Leiden as a risk for developing DVT and CVA. (studyquestions.org)
  • Diagnostic workup of thrombophilia should include screening for FVL, protein C, protein S and AT III deficiency. (studyquestions.org)
  • As part of a signaling pathway known as the RAS/MAPK pathway, the RIT1 protein relays signals from outside the cell to the cell's nucleus. (nih.gov)
  • Tyrosine phosphorylation of the scaffold protein IQGAP1 in the MET pathway alters function. (nih.gov)
  • Our previous study showed that LGR5 functions as a tumor promoter in cervical cancer by activating the Wnt/ β -catenin pathway. (nature.com)
  • 100 U/kg/24 hours of activated prothrombin complex concentrate (aPCC) was administered for 24 hours or more to patients receiving HEMLIBRA prophylaxis. (nih.gov)
  • The abnormally active protein alters normal RAS/MAPK signaling and leads to abnormal cell proliferation, which disrupts the development of organs and tissues throughout the body, resulting in the signs and symptoms of Noonan syndrome. (nih.gov)
  • Salmonella enterica serotype Typhimurium usurps the scaffold protein IQGAP1 to manipulate Rac1 and MAPK signalling. (nih.gov)
  • The work-up also included fibrinogen level, factors VII and VIII activities, lupus anticoagulant and anticardiolipin/antiphospholipid antibodies, antithrombin III, protein S and protein C. DNA was extracted from the sample according to the extraction protocol supplied by the manufacturer (factor V StripAssay, ViennaLab, Austria). (who.int)
  • In this case, protein C functions as an anticoagulant by irreversibly proteolytically inactivating Factor Va and Factor VIIIa, turning them into Factor Vi and Factor VIIIi respectively. (studyquestions.org)
  • People with APC resistance and initial DVT are treated with a standard anticoagulant regimen, for instance intravenous heparin therapy followed by oral anticoagulation. (studyquestions.org)
  • Activated protein C is an anticoagulant plasma protease enzyme that inactivates Factors V and VIII in plasma. (studyquestions.org)
  • But in this case, the first step to turn on the DNA repair response was not about activating certain genes that produce certain proteins. (newswise.com)
  • Resistance to activated protein C due to factor V R506Q mutation as a cause of venous thrombosis. (nih.gov)
  • 7. Effects of hereditary and acquired risk factors of venous thrombosis on a thrombin generation-based APC resistance test. (nih.gov)
  • 12. Resistance to activated protein C caused by the R506Q mutation in the gene for factor V is a common risk factor for venous thrombosis. (nih.gov)
  • Congenital protein C deficiency is one of several inherited thrombophilias, which are a heterogeneous group of genetic disorders associated with an elevated risk of venous thromboembolism. (studyquestions.org)
  • The condition results in a factor V variant that cannot be as easily degraded by activated protein C. The gene that codes the protein is referred to as F5.https://en.wikipedia.org › wiki › Factor_V_LeidenFactor V Leiden - Wikipedia, has been identified as the most common inherited risk factor for venous thrombosis. (studyquestions.org)
  • The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance. (nih.gov)
  • Tissue plasminogen activators, streptokinase and urokinase, activate plasminogen into active plasmin, which further degrade fibrin in the blood clots. (hindawi.com)
  • Another potent thrombolytic agent lumbrokinase of the earth worm Lumbricus and lumbrokinase-like proteins degrade fibrin directly [ 8 - 10 ]. (hindawi.com)
  • In this way, the UPR and ER-phagy work together to refold or degrade damaged proteins and to expand or shrink the ER as needed. (db-engine.de)
  • T2D is characterized by insulin resistance (IR) through which insulin target tissue is unable to respond normally to insulin reflecting insulin deficiency ( 13 ). (frontiersin.org)
  • Protein C deficiency is a congenital or acquired condition that leads to increased risk for thrombosis. (studyquestions.org)
  • Protein S deficiency can affect anyone who has the genetic mutation, regardless of gender. (studyquestions.org)
  • Is factor V Leiden a protein C deficiency? (studyquestions.org)
  • How does protein C deficiency cause thrombosis? (studyquestions.org)
  • Inherited protein C deficiency is caused by mutations in the gene that provides instructions for making protein C, called the PROC gene. (studyquestions.org)
  • If you have too little protein C (protein C deficiency), it means that your blood may clot too much. (studyquestions.org)
  • The RIT1 gene mutations associated with Noonan syndrome change single protein building blocks (amino acids) in the RIT1 protein. (nih.gov)
  • The mutations lead to the production of an altered RIT1 protein that is either continuously turned on (active) or has prolonged activation, rather than promptly switching on and off in response to other cellular proteins. (nih.gov)
  • Similar to the RIT1 gene mutations that cause Noonan syndrome (described above), the mutations involved in these cancers likely result in a constitutively active protein. (nih.gov)
  • In particular, acquisition of macrophage tropism for a serotype 2 FCoV has previously been mapped to the spike gene ( 16 ), further suggesting that key mutations within spike protein may be important for the biotype switch. (cdc.gov)
  • Several mechanisms of resistance to hormonal-therapy have been proposed, [ 23 ] and include the following: downregulation of ER expression, ER mutations, altered expression of ER coregulators, and ligand-independent activation of ER and coactivators by growth factor receptor kinases. (medscape.com)
  • Some of these mutations will confer bacteria resistance to cipro. (newswise.com)
  • Interestingly, the mutations also induce resistance to two other antibiotic drugs the bacteria have not seen before," Zhai said. (newswise.com)
  • 19. Regulation of thrombin formation by activated protein C: effect of the factor V Leiden mutation. (nih.gov)
  • It is activated on the endothelial surface by the thrombin-thrombomodulin complex. (studyquestions.org)
  • 5. Congenital and acquired activated protein C resistance. (nih.gov)
  • The RIT1 gene provides instructions for making a protein that helps cells survive during periods of cellular stress, such as unusually high energy demands. (nih.gov)
  • To transmit signals during periods of cellular stress, the RIT1 protein is turned on by attaching (binding) to a molecule of GTP. (nih.gov)
  • Because FCoV spike protein plays critical roles in receptor binding (S1) and fusion (S2), we focused on structural changes in this protein and potential role in altered cellular tropism. (cdc.gov)
  • The coronavirus spike protein is a class I fusion protein, which typically requires activation by cellular proteases. (cdc.gov)
  • The low-intensity exercise produced increases in protein synthesis, and activated two cellular pathways that stimulate protein synthesis and muscle growth in the post-exercise period. (ironmagazine.com)
  • RNA polymerase is key to protein synthesis. (newswise.com)
  • The ER is a morphologically complex organelle with vital functions in protein folding and lipid synthesis. (db-engine.de)
  • Muscle protein synthesis was measured in each of the men by monitoring changes in a chemical tracer infused into the bloodstream. (ironmagazine.com)
  • Calorie restriction activates AMPK, whereas excess calorie intake inhibits AMPK. (drsears.com)
  • The inhibition of AMPK leads to insulin resistance, which is the first step in developing many chronic disease conditions such as diabetes, heart disease, and neurological diseases such as Alzheimer's. (drsears.com)
  • FAAH is a protein that breaks down anandamide, also known as the "bliss molecule," which is a neurotransmitter that binds to cannabinoid receptors. (scientificamerican.com)
  • IQGAP1 binds to Yes-associated protein (YAP) and modulates its transcriptional activity. (nih.gov)
  • IQGAP1 binds human epidermal growth factor receptor 2 (HER2) and modulates trastuzumab resistance. (nih.gov)
  • PD-L1 protein binds to T cell B7-1/CD80 and PD-1. (rndsystems.com)
  • This enzyme binds to DNA and transcribes DNA-encoded instructions into an RNA sequence, which is then translated into a protein. (newswise.com)
  • ArsR binds to the promoter sequence in the absence of As and releases on binding of As, thereby activating transcription. (igem.org)
  • Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance," he added. (medindia.net)
  • Normal plasma contains a protein that inhibits activated protein C and that is distinct from previously described plasma protease inhibitors. (studyquestions.org)
  • The negative transcriptional regulator ArsR fused with Maltose Binding Protein (MBP) for higher stability. (igem.org)
  • Promoter sequence with recognition site for ArsR transcriptional regulator protein. (igem.org)
  • Promoter sequence containing the recognition site for ArsR transcriptional regulator protein. (igem.org)
  • Double-strand break repair capacity is recognized as an important mechanism in drug resistance and is therefore a potential target for adjuvant chemotherapy. (nih.gov)
  • This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumor and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer," he added. (medindia.net)
  • For example, TB drug resistance is significantly affected by efflux pumps, transporters that sit in the inner membrane of the bacteria and get rid of toxic metabolic byproducts. (seattlechildrens.org)
  • These efflux pumps are often activated in drug resistance," Grundner said. (seattlechildrens.org)
  • Most importantly, the researchers aim to comprehend the function of these transporters in drug resistance. (seattlechildrens.org)
  • There are some indications that these transporters may really play an important role in drug resistance so we want to test that and understand in what ways they affect treatment and resistance," Grundner said. (seattlechildrens.org)
  • 20. Activated protein C resistance assay detects thrombotic risk factors other than factor V Leiden. (nih.gov)
  • The present study investigated the effects of hispidin on palmitate‑induced insulin resistance in C2C12 skeletal muscle myotubes via an MTT assay, glucose uptake assay, Oil‑Red‑O staining and western blot analysis. (spandidos-publications.com)
  • These are some of the same receptors that are activated by marijuana. (scientificamerican.com)
  • Secreted by the acidophil cells of the anterior pituitary, circulating GH shoots to the liver where it can bind GH receptors to stimulate the expression of IGF-I and its cohort IGFBP3 (IGF binding protein 3, there are six in total), a protein that carries IGF-I and magnifies its effects. (bodybuilding.com)
  • 2. Activated protein C resistance and thrombosis: molecular mechanisms of hypercoagulable state due to FVR506Q mutation. (nih.gov)
  • 9. Resistance to activated protein C as risk factor for thrombosis: molecular mechanisms, laboratory investigation, and clinical management. (nih.gov)
  • 13. Activated protein C resistance: molecular mechanisms. (nih.gov)
  • Related mechanisms cooperate with the UPR to clear troublesome proteins, including proteasome biogenesis ( Schmidt et al, 2019 ). (db-engine.de)
  • This membrane protein mediates the uptake of copper (Cu) and zinc (Zn). (igem.org)
  • To answer these questions, we investigate three related processes: (1) ER membrane biogenesis, which enables organelle expansion and remodeling, (2) ER-phagy, which mediates autophagic organelle degradation, and (3) SHRED, which regulates proteasomal degradation of misfolded cytosolic and ER membrane proteins. (db-engine.de)
  • The findings, published in the journal PLOS Biology , identified a new and unusual protein transporter, the PE15/PPE20 complex, that moves calcium - an essential nutrient for many organisms - across the cell's outer membrane. (seattlechildrens.org)
  • Insulin supresses transcriptional activity of yes-associated protein in insulin target cells. (nih.gov)
  • Ozdemir ES, Jang H, Gursoy A, Keskin O, Li Z , Sacks DB, Nussinov R. Unraveling the molecular mechanism of interactions of the Rho GTPases Cdc42 and Rac1 with the scaffolding protein IQGAP2. (nih.gov)
  • Looking to contribute a solution to this growing problem, researchers at Baylor College of Medicine have been studying the process that drives antibiotic resistance at the molecular level. (newswise.com)
  • They report in the journal Molecular Cell crucial and surprising first steps that promote resistance to ciprofloxacin, or cipro for short, one of the most commonly prescribed antibiotics. (newswise.com)
  • Grundner and his team plan to test other proteins in this sub-family to see if they also work as transporters and to determine if they transport just a single nutrient or several, as well as further investigating their molecular structure. (seattlechildrens.org)
  • 3. Expression of the normal factor V allele modulates the APC resistance phenotype in heterozygous carriers of the factor V Leiden mutation. (nih.gov)
  • 17. Activated protein C resistance--a major risk factor for thrombosis. (nih.gov)
  • Activated protein C resistance results in hypercoagulability and an increased risk of deep vein thrombosis. (studyquestions.org)
  • Although HR positivity predicts efficacy of endocrine agents, preclinical and clinical data suggest that HER2 overexpression confers intrinsic resistance to hormonal treatment. (medscape.com)
  • Other factors that may promote DVT are the pres- present with unilateral swollen and oedematous ence of genetic clotting defects due to activated leg. (who.int)
  • Promoter sequence with recognition site for the CueR transcription regulating protein. (igem.org)
  • It suppresses T cell activation and proliferation and induces the apoptosis of activated T cells. (rndsystems.com)
  • Misfolded proteins activate the unfolded protein response (UPR), which increases the protein folding capacity of the ER and induces ER-associated degradation. (db-engine.de)
  • Au nom des organisateurs de PSDI et de son Comité exécutif, nous avons le plaisir de vous accueillir à la 26 ème edition de la conference "Protein Structure Determination in Industry" , qui aura lieu à Versailles , en France, du dimanche 11 au mardi 13 novembre 2018 . (synchrotron-soleil.fr)
  • Many tumors overexpress PD-L1 protein making the PD-1:PD-L1 interaction central to several successful cancer immunotherapy approaches. (rndsystems.com)
  • These data provided a strong rationale for exploring the targeting of both HR and HER2 signaling pathways in HR + /HER2 + breast tumors to optimize hormonal therapy and overcome resistance to anti-estrogen therapy. (medscape.com)
  • Furthermore, even those tumors that initially respond to AIs eventually develop resistance, which leads to disease progression and ultimately to patient death. (medscape.com)
  • Exactly how restricting blood flow in the muscles generated these effects remains unknown, although Rasmussen and Fry speculated that either an improved ability to activate Type II muscle fibers or a response to the sudden surge of blood into the muscles when the cuffs were released could be responsible. (ironmagazine.com)
  • Now, though, University of Texas Medical Branch at Galveston researchers have determined that moderately and temporarily restricting the flow of blood through muscles - a practice adopted by bodybuilders who noticed that it made light weights feel heavier - can be combined with low-level resistance exercise training to produce muscle-mass increases in older men. (ironmagazine.com)
  • These proteins play important roles in cell division, cell differentiation, and the self-destruction of cells (apoptosis). (nih.gov)
  • We discuss the clinical implication of resistance to endocrine therapy, and describe new insights into the management of HR + /HER2 + advanced breast cancer. (medscape.com)
  • There is the need to study the ailment in protein C resistance (factor V Leiden muta- greater detail. (who.int)
  • 15. Factor V and protein S as cofactors to activated protein C. (nih.gov)
  • Sharma S, Findlay GM, Bandukwala HS, Oberdoerffer S, Baust B, Li Z , Schmidt V, Hogan PG, Sacks DB, Rao A. Dephosphorylation of the nuclear factor of activated T cells (NFAT) transcription factor is regulated by an RNA-protein scaffold complex. (nih.gov)
  • Excessive saturated fatty acids are considered to be a major contributing factor to insulin resistance in skeletal muscle cells. (spandidos-publications.com)
  • During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. (medindia.net)
  • Does protein C inactivate Factor 5? (studyquestions.org)
  • Is factor V Leiden a protein? (studyquestions.org)
  • Does protein C inhibit factor V? (studyquestions.org)
  • Is Factor V Leiden the same as activated protein C resistance? (studyquestions.org)
  • While resistance to APC is most commonly caused by the presence of factor V Leiden, the results of the clotting test for resistance to APC can be positive without factor V Leiden. (studyquestions.org)
  • What does protein C do to Factor 5? (studyquestions.org)
  • PD-L1 is expressed on inflammatory-activated immune cells including macrophages, T cells, and B cells, keratinocytes, enothelial and intestinal epithelial cells, as well as a variety of carcinomas and melanoma. (rndsystems.com)
  • 4. Early days of APC resistance and FV Leiden. (nih.gov)
  • Can weight loss or other clinical interventions improve abnormal metabolic profiles (i.e., insulin resistance) and modify cancer risk? (nih.gov)
  • If protein C cannot control blood clotting, abnormal blood clots may form. (studyquestions.org)
  • When the protein is bound to GDP, it does not relay signals to the cell's nucleus. (nih.gov)
  • ZntR activates transcription when Zn(II) is bound. (igem.org)
  • The findings point at potential strategies that could prevent bacteria from developing resistance, extending the effectiveness of new and old antibiotics. (newswise.com)
  • Together with a previous study on three related transporters, this work suggests a family-wide function of the nearly 170 proteins and provides a likely answer of how the bacteria takes up nutrients. (seattlechildrens.org)
  • In cancer, PD-L1 provides resistance to T cell mediated lysis, enhances EMT, and enhances the tumorigenic function of Th22 cells. (rndsystems.com)
  • When copper levels in the cell rise CueR activates transcription. (igem.org)
  • Try to imagine a small population of little water sacs (satellite cells) sitting on top of a huge self-sealing water balloon (muscle cell), constantly dividing (mitosis), growing, becoming activated, and fusing with the balloon to spill their soggy contents and form an ever-larger one (hypertrophy of a multinucleate muscle cell). (bodybuilding.com)
  • Thrombolytic therapy with t-PA at present is limited by the relatively high incidence of reocclusion and resistance to reperfusion, despite therapeutic heparinization [ 7 , 8 ]. (hindawi.com)
  • 4 Previous studies have suggested that only a rare subpopulation of tumor cells called cancer stem cells (CSCs) can regenerate the tumor and may be involved in therapy resistance, tumor relapse and metastasis. (nature.com)
  • Usually, cells regulate their activities by producing specific proteins that mediate the desired function. (newswise.com)
  • Through micro-ER-phagy, cells may sacrifice parts of their ER to destroy protein aggregates. (db-engine.de)
  • With less FAAH activity, this patient was found to have more circulating levels of anandamide, which may explain her resistance to feeling pain. (scientificamerican.com)
  • Instead, the first step consisted of disrupting the activity of a protein already present, RNA polymerase. (newswise.com)
  • In general terms, this indicates that a resistance activity for the leg musculature does not result in adaptation in the arm musculature. (bodybuilding.com)
  • What is protein C activity mean? (studyquestions.org)
  • Absence of IQGAP1 protein leads to insulin resistance. (nih.gov)
  • The UTMB investigators studied changes in the thigh muscles of seven older men (average age 70) when they performed four minutes of low-resistance leg extension exercises both with and without inflatable cuffs that reduced blood flow out of the muscles. (ironmagazine.com)
  • This test measures the level of protein C in your blood. (studyquestions.org)
  • Protein C helps your blood clot normally. (studyquestions.org)