Search results

1

In vitro expression analysis of R68G and R68S mutations in phenylalanine hydroxylase gene.

100%

Żekanowski C., Perez B., Desviat L. R., Wiszniewski W., Ugarte M.

|

2000

|

vol. 47

|

issue 2

365-369

EN

Phenylketonuria (PKU), an autosomal recessive disorder caused be a deficiency of hepatic phenylalanine hydroxylase (PAH), is clinically very heterogeneous. At the molecular level, more than 400 mutations in the PAH gene are known to date, which in different genotype combinations could account for biochemical and clinical variability of symptoms. In vitro expression studies on R68G and R68S mutations causing mild phenylketonuria are presented.

2

The effect of Arg209 to Lys mutation in mouse thymidylate synthase.

100%

Cieśla J., Gołos B., Wałajtys-Rode E., Jagielska E., Płucienniczak A., Rode W.

|

2002

|

vol. 49

|

issue 3

651-658

EN

Mouse thymidylate synthase R209K (a mutation corresponding to R218K in Lactobacillus casei), overexpressed in thymidylate synthase-deficient Escherichia coli strain, was poorly soluble and with only feeble enzyme activity. The mutated protein, incubated with FdUMP and N5,10-methylenetetrahydrofolate, did not form a complex stable under conditions of SDS/polyacrylamide gel electrophoresis. The reaction catalyzed by the R209K enzyme (studied in a crude extract), compared to that catalyzed by purified wild-type recombinant mouse thymidylate synthase, showed the Km value for dUMP 571-fold higher and Vmax value over 50-fold (assuming that the mutated enzyme constituted 20% of total crude extract protein) lower. Thus the ratios kcat, R209K/kcat, 'wild' and (kcat, R209K/Km, R209KdUMP)/( kcat, 'wild'/Km, 'wild'dUMP) were 0.019 and 0.000032, respectively, documenting that mouse thymidylate synthase R209, similar to the corresponding L. casei R218, is essential for both dUMP binding and enzyme reaction.

3

Mutations in type I collagen genes resulting in osteogenesis imperfecta in humans.

100%

Gajko-Galicka A.

|

EN

Osteogenesis imperfecta (OI), commonly known as "brittle bone disease", is a dominant autosomal disorder characterized by bone fragility and abnormalities of connective tissue. Biochemical and molecular genetic studies have shown that the vast majority of affected individuals have mutations in either the COL1A1 or COL1A2 genes that encode the chains of type I procollagen. OI is associated with a wide spectrum of phenotypes varying from mild to severe and lethal conditions. The mild forms are usually caused by mutations which inactivate one allele of COL1A1 gene and result in a reduced amount of normal type I collagen, while the severe and lethal forms result from dominant negative mutations in COL1A1 or COL1A2 which produce structural defects in the collagen molecule. The most common mutations are substitutions of glycine residues, which are crucial to formation and function of the collagen triple helix, by larger amino acids. Although type I collagen is the major structural protein of both bone and skin, the mutations in type I collagen genes cause a bone disease. Some reports showed that the mutant collagen can be expressed differently in bone and in skin. Since most mutations identified in OI are dominant negative, the gene therapy requires a fundamentally different approach from that used for genetic-recessive disorders. The antisense therapy, by reducing the expression of mutant genes, is able to change a structural mutation into a null mutation, and thus convert severe forms of the disease into mild OI type I.

4

Biochemical characterization of a catalase from Vibrio vulnificus, a pathogen that causes gastroenteritis

88%

Pei J., Wang H., Wu L., Xia S., Xu C., Zheng B., Li T., Jiang Y.

|

2017

|

vol. 64

|

issue 3

543-549

EN

Vibrio vulnificus is a virulent human pathogen causing gastroenteritis and possibly life threatening septicemia in patients. Most V. vulnificus are catalase positive and can deactivate peroxides, thus allowing them to survive within the host. In the study presented here, a catalase from V. vulnificus (CAT-Vv) was purified to homogeneity after expression in Escherichia coli. The kinetics and function of CAT-Vv were examined. CAT-Vv catalyzed the reduction of H2O2 at an optimal pH of 7.5 and temperature of 35°C. The Vmax and Km values were 65.8±1.2 U/mg and 10.5±0.7 mM for H2O2, respectively. Mutational analysis suggests that amino acids involved in heme binding play a key role in the catalysis. Quantitative reverse transcription-PCR revealed that in V. vulnificus, transcription of CAT-Vv was upregulated by low salinity, heat, and oxidative stresses. This research gives new clues to help inhibit the growth of, and infection by V. vulnificus.

5

A novel homozygous mutation in the WNK1/HSN2 gene causing hereditary sensory neuropathy type 2

88%

Potulska-Chromik A., Kabzińska D., Lipowska M., Kostera-Pruszczyk A., Kochański A.

|

2012

|

vol. 59

|

issue 3

413-415

EN

Hereditary sensory and autonomic neuropathy type 2 is a rare disorder caused by recessive mutations in the WNK1/HSN2 gene located on chromosome 12p13.33. Phenotype of the patients is characterized by severe sensory loss affecting all sensory modalities. We report a novel homozygous Lys179fsX182 (HSN2); Lys965fsX968 (WNK1/HSN2) mutation causing an early childhood onset hereditary sensory and autonomic neuropathy type 2, with acromutilations in upper and lower limbs, and autonomic dysfunction. To the best of our knowledge this is the first genetically proven case of hereditary sensory and autonomic neuropathy type 2 originating from East Europe.

6

Mutations in the COL1A1 and COL1A2 genes associated with osteogenesis imperfecta (OI) types I or III

88%

Augusciak-Duma A., Witecka J., Sieron A., Janeczko M., Pietrzyk J., Ochman K., Galicka A., Borszewska-Kornacka M., Pilch J., Jakubowska-Pietkiewicz E.

|

2018

|

vol. 65

|

issue 1

79-86

EN

Although over 85% of osteogenesis imperfecta (OI) cases are associated with mutations in the procollagen type I genes (COL1A1 or COL1A2), no hot spots for the mutations were associated with particular clinical phenotypes. Eight patients that were studied here, diagnosed with OI by clinical standards, are from the Polish population with no ethnic background indicated. Previously unpublished mutations were found in six out of those eight patients. Genotypes for polymorphisms (Sp1 - rs1800012 and PvuII - rs412777), linked to bone formation and metabolism were determined. Mutations were found in exons 2, 22, 50 and in introns 13 and 51 of the COL1A1 gene. In COL1A2, one mutation was identified in exon 22. Deletion type mutations in COL1A1 that resulted in OI type I had no effect on collagen type I secretion, nor on its intracellular accumulation. Also, a single base substitution in I13 (c.904-9 G>T) was associated with the OI type I. The OI type III was associated with a single base change in I51 of COL1A1, possibly causing an exon skipping. Also, a missense mutation in COL1A2 changing Gly→Cys in the central part of the triple helical domain of the collagen type I molecule caused OI type III. It affected secretion of the heterotrimeric form of procollagen type I. However, no intracellular accumulation of procollagen chains could be detected. Mutation in COL1A2 affected its incorporation into procollagen type I. The results obtained shall help in genetic counseling of OI patients and provide a rational support for making informed, life important decisions by them and their families.

7

Production, characterization and iron binding affinity of hydroxamate siderophores from rhizosphere associated fluorescent Pseudomonas

75%

Monali D., Subramanyan J. N., Satyan K. B.

Journal of Plant Protection Research

|

2018

|

vol. 58

|

issue 1

8

Genetic study of familial cases of Alzheimer's disease.

75%

Kowalska A., Pruchnik-Wolińska D., Florczak J., Modestowicz R., Szczech J., Kozubski W., Rossa G., Wender M.

|

vol. 51

|

issue 1

245-242

EN

A small number (1-5%) of Alzheimer's disease (AD) cases associated with the early-onset form of the disease (EOAD) appears to be transmitted as a pure genetic, autosomal dominant trait. To date, three genes responsible for familial EOAD have been identified in the human genome: amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2). Mutations in these genes account for a significant fraction (18 to 50%) of familial cases of early onset AD. The mutations affect APP processing causing increased production of the toxic Aβ42 peptide. According to the "amyloid cascade hypothesis", aggregation of the Aβ42 peptide in brain is a primary event in AD pathogenesis. In our study of twenty AD patients with a positive family history of dementia, 15% (3 of 20) of the cases could be explained by coding sequence mutations in the PS1 gene. Although a frequency of PS1 mutations is less than 2% in the whole population of AD patients, their detection has a significant diagnostic value for both genetic counseling and treatment in families with AD.

9

TP53 and mutations in human cancer.

75%

Szymańska K., Hainaut P.

|

2003

|

vol. 50

|

issue 1

231-238

EN

TP53 is the most frequently mutated gene in human cancer, with a predominance of missense mutations scattered over 200 codons. In many cancers, specific mutation patterns can be identified, which are shaped by site-specific mutagenesis and by biological selection. In tobacco-related cancers (lung, head and neck), organ-specific patterns are observed, with many mutations compatible with the ones experimentally induced by tobacco carcinogens. In several other cancers, such as squamous cell carcinoma of the oesophagus or hepatocellular carcinoma (HCC), mutation patterns show geographic variations between regions of high and low incidence, suggesting a role for region-specific risk factors. HCC from high-incidence regions showing also a high prevalence of a specific Ser-249 TP53 mutation is one of the most striking examples of a mutagen fingerprint. All such assessments are useful to generate clues on the mutagenic mechanisms involved in human cancer. Moreover, it has been shown that DNA retrieved from plasma can be successfully used for detection of TP53 mutations, which gives hope for earlier more accurate detection of human cancers.

10

Znaczenie kwasu foliowego dla zdrowia organizmu człowieka

63%

Banyś K. J., Knopczyk M. W., Bobrowska-Korczak B.

Farmacja Polska

|

2020

|

vol. 76

|

issue 2

79-87

EN

A well-balanced diet is undoubtedly a key factor to maintain your body's normal state of health. A deficiency or excess of any nutrient can cause negative effects on human health. Folic acid is one of the elements of the diet, which is often supplied in insufficient quantities. This vitamin and its derivatives participate in the metabolism of amino acids and nucleic acids. Therefore, it is necessary for the proper functioning of the body's cells and for maintaining homeostasis, especially of the nervous, circulatory and cardiovascular systems. The biological activity of folic acid and its derivatives essentially affects the metabolism of important amino acids, such as methionine, homocysteine, serine, glycine, pyrimidine and purine synthesis and DNA methylation. The synthetic form of folic acid (most oxidized), which can be found in fortified foods, dietary supplements or pharmaceuticals, does not show biological activity. It is transformed in a series of reactions with the participation of many enzymes to form folates, which differ in the number of glutamic acid residues and the degree of oxidation. The actively biological form is reduced folate (L-5-MTHF), which is transported together with the blood to cells where it undergoes biological processes important for our health. The MTHFR gene, coding for the enzyme protein of the same name - methylene tetrahydrofolate reductase, is located on chromosome 1 at the 1p36.3 locus. This protein is responsible for the catalysis of the enzymatic reaction, which is the reduction of 5,10-methylenetetrahydrofolate to L-5-methyltetrahydrofolate, i.e. the active form of folate. This form is necessary in the process of homocysteine degradation, in the aftermath remethylation to methionine. This protein is responsible for the catalysis of the enzymatic reaction, which is the reduction of 5,10-methylenetetrahydrofolate to L-5-methyltetrahydrofolate, i.e. the active form of folate. This form is necessary in the process of homocysteine degradation, in the aftermath remethylation to methionine. However, according to available literature, mutation of the MTHFR 677C> T gene occurs in even 53% of the population. Among carriers of the TT genotype, it can cause about 70% reduction of MTHFR reductase activity. It is especially dangerous for people who do not provide adequate amounts of folic acid along with their diet and for those who need a high amount of this vitamin, e.g. due to taking medications that reduce its absorption, i.e. metformin or oral contraceptives. Many people metabolize folic acid on insufficient levels. For medical reasons, not the mutation itself is a problem, but too low the folate levels. In recent years, there is more and more discussion about the active form of folic acid and the possibility of effective supplementation with metapholine, which is a combination of calcium with L-5-MTHFR. It is a natural and reduced form of folate, which hydrolized and then transforms into L-5-MTHFR. Metapholine, in comparison to folic acid, is not reduced to be incorporated into metabolic processes in the cell, which is catalyzed by DHFR and MTHFR enzymes. In addition, the absorption of the active form of folic acid is faster because some metabolic pathways are missed. This is particularly important for people who have a MTHFR gene mutation homozygous with 665C> T and / or 1298A> C polymorphism and a mutation of the DHFR gene with 458A> T polymorphism. Numerous clinical studies have confirmed the efficacy and safety of the active form of folic acid. In a study by Houghton et al., which was conducted among pregnant Canadian women, L-5-MTHFR was shown to be at least as effective in lowering homocysteine levels as folic acid supplementation. In addition, the active form of folic acid was more effective at storing folate in erythrocytes. In a study conducted by Lamers et al. on 135 women after a period of 24 weeks, L-5MTHR was shown to be a suitable alternative in reducing plasma homocysteine levels compared to folic acid and placebo. In addition, Bentley et al. analyzed the results of 112 pregnant women from the USA. Patients were assigned to two groups in which each took vitamin B12. In addition, in one of them women supplemented with L-5-MTHFR, and in the other - folic acid. The results showed that patients who supplemented the active form of folic acid not only had higher hemoglobin levels, but also less often had anemia. When analyzing clinical trials of patients with the MTHFR mutation, the same trend was observed. Metafoline increased plasma folate levels and decreased homocysteine levels. In one study on German women, there was a decrease in homocysteine levels and an increase in folate levels in both plasma and red blood cells in patients who supplemented the active form of folic acid. In another study involving Swiss patients with the current 677CC MTHFR or 677TT MTHFR mutation, it was demonstrated that using L-5-MTHFR significantly reduces homocysteine levels compared to folic acid. It is also worth mentioning that Prinz-Langenhol et al. in a study on women with the 677CC and 677TT mutations proved that the active form of folic acid has a better effect on increasing folate levels than folate. It is also worth mentioning that folic acid at high doses can mask ailments or even diseases caused by vitamin B12 deficiency. In addition, folic acid administered at high doses in patients with the MTHFR mutation is not reduced to an oxidized, inactive form and is not properly transported to plasma. Non-metabolised folic acid can be dangerous to the human body and contribute to the development of cancer. Supplementation, in particular the active form of folic acid, should be considered by patients who are carriers of the MTHFR or DHFR mutation. In addition, the use of stimulants such as alcohol or nicotine also negatively affects the absorption of this vitamin. Taking some medications weakens the absorption of folic acid - these include folic acid antagonists, anti-tuberculosis drugs, hormonal oral contraceptives, nonsteroidal anti-inflammatory drugs or metformin widely used. Folic acid is necessary for the proper functioning of the human body and its deficiency may induce various disease processes in the body, which include: the formation of neural tube defects, disorders in the nervous system, megaloblastic anemia, a negative effect on the functioning of the cardiovascular system and the development of atherosclerosis and cancer. More and more people have anemia, including megaloblastic anemia, which is characterized by abnormal nucleic acid synthesis. The consequence of too low folate levels is impaired red blood cell production, an increase in their volume, and premature death. Extremely dangerous is megaloblastic anemia, the so-called malignant anemia in pregnant women, as it can lead to serious complications such as hemorrhage, infection, and even intrauterine fetal death. A significant influence of folic acid on the functioning of the nervous system has been proven in many clinical studies. This vitamin is involved in the formation of important neurotransmitters such as: adrenaline, dopamine and noradrenaline, therefore its deficiency may lead to the development of neuropsychiatric disorders (dementia, epilepsy, depression and psychosis). These disorders are often caused by high levels of homocysteine, which is not properly metabolized to methionine due to folate deficiency. An excess of homocysteine, as a consequence, leads to atherosclerosis in the cerebral arteries and, as a result of insufficient blood supply, transient ischaemic attack occur, which can contribute to the development of dementia or Alzheimer's disease. Nutritional observations indicate that eating fresh vegetables rich in folic acid protects against the formation of some cancers, e.g. large intestine, breast, ovary, uterus, lungs, pancreas. Deficiency of folic acid promotes the activation of protooncogenes to oncogenes, which in consequence results in a decrease in the stability of cellular DNA. A study carried out by Giovannicci et al. showed that excessive alcohol consumption and folic acid deficiency associated with it increased the risk of developing colorectal cancer by almost four times. However, what cannot be overlooked, the results of clinical trials show us that very high doses and folic acid accumulation favor the development of some cancers. It is thought that excess of folic acid may lead to hypermethylation of DNA and, consequently, to inactivation of the suppressor genes responsible for controlling cell division. Women in the pre-contraceptive period, during pregnancy and breastfeeding are included in the group of people with a special need for folic acid, in whom deficiency can cause many negative effects. The presence of folic acid is necessary in the process of cell formation and growth in the developing fetus, especially when the neural tube is forming. Moreover adequate folic acid concentration decreases risk of fetal heart and urinary tract defects, and also reduces the occurrence of thrombosis and miscarriage in pregnant women. Steeweg-de Graaff J. et al. conducted evaluation of emotional and behavioral development at the age of 3 depending on the concentration of folates and homocysteine in the mother's blood plasma at an early stage of the pregnancy. It was noted that with insufficient folate supply, associated with a lack of or its late supplementation increases the risk of emotional problems in children. In addition, defects of the nervous system may occur as a result of dysfunction of folate metabolism. In its transformation pathway MTHFR reductase takes a particular role. Its reduced activity contributes to the impairment of folic acid metabolism, and the MTHFR gene - type 677CC is considered a risk factor for the development of neural tube defects. Randomized study compared pharmacokinetic parameters of [6S]-5-MTHF and folic acid in healthy women of childbearing age with different MTHFR genotypes (677TT n = 6, 677CC n = 8). Higher peak folate concentrations in plasma with [6S]-5-MTHF supplementation was found, in comparison with folic acid and not depending in the MTHFR genotype, as well as a shorter time needed to reach maximum concentration. In a different randomized, double-blind trial significantly higher folate levels in red blood cells were obtained in women receiving [6S]-5-MTHF. Studies confirm the hypothesis that nutritional deficiencies are of great importance in terms of fetal development. The results testify the need of folic acid supplementation, in which it is worth to consider the use of biologically active form, 12 weeks before planned pregnancy. In the second and third trimesters, the supplementation of folic acid is an important element in prevention of anemia caused by vitamin B12 and folic acid deficiency, i.e. megaloblastic anemia. Moreover, it was found that folic acid at a daily dose of 400 - 800 μg reduce the risk of fetal neural tube defects. In its guidelines, Polish Society of Gynecologists and Obstetricians (PTGiP) recommends supplementation of 400 μg / day of folic acid in women in low risk group in the pre-contraceptive period, pregnancy and during breastfeeding and supplementation of 800 μg/ day of folic acid in women in intermediate risk group and also high risk group in II and III trimester and during breastfeeding. It is worth emphasising that in most recent guidelines, PTGiP pays attention to the problem of folic acid metabolism and emphasizes the appropriateness of supplementation with its active form, especially at high doses. In folic acid metabolism, MTHFR catalyzes the synthesis to the active form of folate (L-5-MTHFR). It is necessary in the process of homocysteine degradation following remethylation to methionine. Unfortunately, as a result of inappropriate methylation, e.g. as a result of active form of folic acid deficiency, the concentration of homocysteine in the blood serum increases, which is responsible for various pathogenic processes in the body. Insufficient supply and improper metabolism of folic acid, as well as vitamins B6, B12 deficiency may be factors favorable for development of atherosclerosis and other diseases related to the cardiovascular system (e.g. heart attack, stroke, coronary artery disease). Excessively high concentration of homocysteine in the blood plasma, caused by disorders of its metabolic pathway in the body, is one of the reasons for the formation of atherosclerotic changes in blood vessels. Excess of homocysteine, with a simultaneous deficiency of folate and vitamin B12, damages the endothelium of blood vessels and increases oxidation processes, which are associated with the development of inflammation, oxidation of LDL cholesterol and change in the structure of the walls of blood vessels. In addition, the risk of developing peripheral thrombosis and hypertension increases. In the meta-analysis of Linda L. et al. it was found that high concentration of homocysteine is an independent factor of developing coronary heart disease. In the majority of studies, the risk of this disease is increased by 20% to 50% with every increase of concentration of homocysteine by 5 μmol /L in the blood of the examined persons. To ensure proper functioning of blood vessels and to reduce the risk of cardiovascular disease, one needs to provide adequate concentration of homocysteine in the body. Folates and their adequate supply with diet or supplementation play a key role in this process. Looking at the numerous clinical studies, available literature and the function of folic acid, it can be stated that it is an essential compound with multidirectional biological action, which is involved in the synthesis of amino acids and nucleic acids important for health. It plays an important role in tissues, such as: the fetus, hematopoietic system and gastrointestinal epithelium, in which cell divisions occur. For this reason, the presence of folic acid in the right amounts, ensures the proper functioning of our body. A deficiency of folic acid in the diet leads to a reduced concentration of folate in plasma and red blood cells. It is a condition that contributes to the formation of many serious diseases in our body and congenital neural tube defects in the fetus. As clinical studies have shown, the optimal concentration of folates in the blood reduces the risk of cardiovascular, circulatory, central nervous system diseases and certain types of cancer. To reduce the risk of diet-related diseases caused by folic acid deficiency, daily diet should be optimally balanced and contain products rich in natural folates. If diet is an insufficient source of folic acid, its supplementation should be considered, with the possible inclusion of its active form. Supplementation is recommended, in particular, for people with: megaloblastic anemia, diabetes mellitus, malabsorptions (e.g. Crohn's disease), alcoholism, malnutrition, neurodegenerative diseases (e.g. Alzheimer's disease), cardiovascular diseases, elevated homocysteine levels and using certain medications (e.g. oral contraceptives, metformin, methotrexate). It is also worth mentioning that metapholine supplementation bypasses the multistage metabolic process before incorporating folates into the cell cycle, as opposed to the inactive form of folic acid. This is particularly important for patients with the DHFR and MTHFR mutation, which depending on the polymorphism, may occur in up to 53% of the Caucasian population. Consequently, MTHFR reductase activity is reduced by up to 70%.

PL

Kwas foliowy jest niezbędny do właściwego funkcjonowania organizmu i zachowania homeostazy. Uczestniczy w metabolizmie kwasów nukleinowych, aminokwasów, syntezie pirymidyn i puryn. Syntetyczna postać kwasu foliowego nie wykazuje aktywności biologicznej. Przekształcana jest w szeregu reakcji do postaci folianów (L-5-MTHF) które, są transportowane do komórek, gdzie bierze udział w ważnych procesach biologicznych. Gen MTHFR odpowiedzialny jest za katalizę reakcji enzymatycznej: redukcję 5,10-metylenotetrahydrofolianu do aktywnej formy. Mutacja genu MTHFR 677C>T występuje nawet u 53% populacji czego konsekwencją jest zmniejszenie aktywności reduktazy – MTHFR nawet o 70%. Metafolina (aktywna forma) w przeciwieństwie do kwasu foliowego, aby zostać włączona do procesów metabolicznych w komórce, nie ulega redukcji, katalizowanej przez DHFR oraz MTHFR. Jest to istotne w szczególności dla osób, które mają mutację genu MTHFR oraz DHFR. Przyjmowanie niektórych leków osłabia wchłanialność kwasu foliowego. Kwas foliowy jest niezbędny do prawidłowego funkcjonowania organizmu człowieka a jego niedobór może indukować różne procesy chorobowe w organizmie, do których zaliczamy: powstawanie wad cewy nerwowej, zaburzenia w układzie nerwowym, niedokrwistość megaloblastyczną, negatywny wpływ na funkcjonowanie układu sercowo – naczyniowego oraz rozwój miażdżycy i nowotworów. Witamina ta bierze udział w powstawaniu ważnych neuroprzekaźników, takich jak: adrenalina, dopamina i noradrenalina, dlatego jej niedobór może prowadzić do powstania zaburzeń neuropsychiatrycznych. Niedobór kwasu foliowego sprzyja aktywacji protoonkogenów do onkogenów. Liczne badania kliniczne i dostępna literatura potwierdzają funkcję kwasu foliowego, że jest to niezbędny związek o wielokierunkowym działaniu biologicznym, który pełni istotną rolę w tkankach. Suplementacja metafoliną omija wieloetapowy proces metaboliczny w przeciwieństwie do nieaktywnej postaci kwasu foliowego.

11

Directionality of kinesin motors.

63%

Kasprzak A. A., Hajdo Ł.

|

2002

|

vol. 49

|

issue 4

813-821

EN

Kinesins are molecular motors that transport various cargoes along microtubule tracks using energy derived from ATP hydrolysis. Although the motor domains of kinesins are structurally similar, the family contains members that move on microtubules in opposite directions. Recent biochemical and biophysical studies of several kinesins make it possible to identify structural elements responsible for the different directionality, suggesting that reversal of the motor movement can be achieved through small, local changes in the protein structure.

12

The present state of herbicide resistance of weed populations in the Czech Republic

63%

Salava J., Chodová D.

Journal of Plant Protection Research

|

2007

|

vol. 47

|

issue 4

Refine search results

In vitro expression analysis of R68G and R68S mutations in phenylalanine hydroxylase gene.

The effect of Arg209 to Lys mutation in mouse thymidylate synthase.

Mutations in type I collagen genes resulting in osteogenesis imperfecta in humans.

Biochemical characterization of a catalase from Vibrio vulnificus, a pathogen that causes gastroenteritis

A novel homozygous mutation in the WNK1/HSN2 gene causing hereditary sensory neuropathy type 2

Mutations in the COL1A1 and COL1A2 genes associated with osteogenesis imperfecta (OI) types I or III

Production, characterization and iron binding affinity of hydroxamate siderophores from rhizosphere associated fluorescent Pseudomonas

Genetic study of familial cases of Alzheimer's disease.

TP53 and mutations in human cancer.

Znaczenie kwasu foliowego dla zdrowia organizmu człowieka

Directionality of kinesin motors.

The present state of herbicide resistance of weed populations in the Czech Republic