Sequence Homology, Amino Acid
Amino Acid Sequence
Amino Acids
Sequence Homology, Nucleic Acid
Molecular Sequence Data
Cloning, Molecular
Base Sequence
Sequence Alignment
Amino Acid Substitution
Sequence Homology
Escherichia coli
DNA, Complementary
Binding Sites
DNA
Models, Molecular
Restriction Mapping
Mutation
Protein Structure, Tertiary
Genes
Protein Conformation
Amino Acids, Essential
Amino Acid Motifs
Sequence Analysis, DNA
Amino Acid Transport Systems
Peptide Fragments
Plasmids
Protein Binding
Species Specificity
Mutagenesis, Site-Directed
RNA, Messenger
Substrate Specificity
Nucleic Acid Hybridization
Conserved Sequence
Open Reading Frames
Structure-Activity Relationship
Peptides
Recombinant Fusion Proteins
DNA Restriction Enzymes
Proteins
Carrier Proteins
Gene Library
Electrophoresis, Polyacrylamide Gel
Protein Structure, Secondary
Transcription, Genetic
DNA Primers
Polymerase Chain Reaction
Multigene Family
Saccharomyces cerevisiae
Cattle
Structural Homology, Protein
Blotting, Northern
Membrane Proteins
Cyanogen Bromide
Trypsin
src Homology Domains
Chromatography, High Pressure Liquid
Chromosome Mapping
Transfection
Codon
Blotting, Southern
Plant Proteins
Sequence Analysis
Protein Biosynthesis
Gene Expression
DNA-Binding Proteins
Alanine
Macromolecular Substances
Genetic Complementation Test
Sequence Analysis, Protein
Mutagenesis
Biological Evolution
Repetitive Sequences, Nucleic Acid
Evolution, Molecular
COS Cells
Biological Transport
Crystallography, X-Ray
Chickens
Rabbits
RNA
Transcription Factors
Proline
Plants
Amino Acid Transport Systems, Basic
Point Mutation
Endopeptidases
Oligonucleotide Probes
Isoleucine
Catalysis
Glycine
Consensus Sequence
Promoter Regions, Genetic
Nucleic Acid Conformation
Chymotrypsin
Cricetinae
Liver
Swine
Chromatography, Gel
Protein Sorting Signals
Cell Membrane
Saccharomyces cerevisiae Proteins
DNA, Recombinant
Gene Expression Regulation
Peptide Mapping
Aspartic Acid
Chromatography, Ion Exchange
HeLa Cells
Cross Reactions
Serine Endopeptidases
Phenotype
Oligodeoxyribonucleotides
Cells, Cultured
Tissue Distribution
Exons
Glutamine
Catalytic Domain
Glycoproteins
Circular Dichroism
Tryptophan
Valine
Gene Expression Regulation, Bacterial
Operon
Dimerization
Organ Specificity
Mass Spectrometry
Protein Processing, Post-Translational
Temperature
DNA Transposable Elements
Phosphorylation
Hydrogen-Ion Concentration
Excitatory Amino Acids
Cercopithecus aethiops
Phenylalanine
Nitrogen
Nuclear Proteins
Isoenzymes
Repetitive Sequences, Amino Acid
Serine
Xenopus laevis
Threonine
Recombination, Genetic
Signal Transduction
Tyrosine
Mutagenesis, Insertional
Genetic Code
Blotting, Western
Amino Acid Transport System A
Chromatography, Affinity
Glycosylation
Gene Deletion
Genomic Library
Binding, Competitive
Magnetic Resonance Spectroscopy
Introns
Enzyme Stability
Ligands
Immunoblotting
Blood Proteins
Amino Acyl-tRNA Synthetases
CHO Cells
Glutathione Transferase
Disulfides
Computational Biology
Novel regulation of the homeotic gene Scr associated with a crustacean leg-to-maxilliped appendage transformation. (1/50418)
Homeotic genes are known to be involved in patterning morphological structures along the antero-posterior axis of insects and vertebrates. Because of their important roles in development, changes in the function and expression patterns of homeotic genes may have played a major role in the evolution of different body plans. For example, it has been proposed that during the evolution of several crustacean lineages, changes in the expression patterns of the homeotic genes Ultrabithorax and abdominal-A have played a role in transformation of the anterior thoracic appendages into mouthparts termed maxillipeds. This homeotic-like transformation is recapitulated at the late stages of the direct embryonic development of the crustacean Porcellio scaber (Oniscidea, Isopoda). Interestingly, this morphological change is associated with apparent novelties both in the transcriptional and post-transcriptional regulation of the Porcellio scaber ortholog of the Drosophila homeotic gene, Sex combs reduced (Scr). Specifically, we find that Scr mRNA is present in the second maxillary segment and the first pair of thoracic legs (T1) in early embryos, whereas protein accumulates only in the second maxillae. In later stages, however, high levels of SCR appear in the T1 legs, which correlates temporally with the transformation of these appendages into maxillipeds. Our observations provide further insight into the process of the homeotic leg-to-maxilliped transformation in the evolution of crustaceans and suggest a novel regulatory mechanism for this process in this group of arthropods. (+info)The Drosophila kismet gene is related to chromatin-remodeling factors and is required for both segmentation and segment identity. (2/50418)
The Drosophila kismet gene was identified in a screen for dominant suppressors of Polycomb, a repressor of homeotic genes. Here we show that kismet mutations suppress the Polycomb mutant phenotype by blocking the ectopic transcription of homeotic genes. Loss of zygotic kismet function causes homeotic transformations similar to those associated with loss-of-function mutations in the homeotic genes Sex combs reduced and Abdominal-B. kismet is also required for proper larval body segmentation. Loss of maternal kismet function causes segmentation defects similar to those caused by mutations in the pair-rule gene even-skipped. The kismet gene encodes several large nuclear proteins that are ubiquitously expressed along the anterior-posterior axis. The Kismet proteins contain a domain conserved in the trithorax group protein Brahma and related chromatin-remodeling factors, providing further evidence that alterations in chromatin structure are required to maintain the spatially restricted patterns of homeotic gene transcription. (+info)The homeobox gene Pitx2: mediator of asymmetric left-right signaling in vertebrate heart and gut looping. (3/50418)
Left-right asymmetry in vertebrates is controlled by activities emanating from the left lateral plate. How these signals get transmitted to the forming organs is not known. A candidate mediator in mouse, frog and zebrafish embryos is the homeobox gene Pitx2. It is asymmetrically expressed in the left lateral plate mesoderm, tubular heart and early gut tube. Localized Pitx2 expression continues when these organs undergo asymmetric looping morphogenesis. Ectopic expression of Xnr1 in the right lateral plate induces Pitx2 transcription in Xenopus. Misexpression of Pitx2 affects situs and morphology of organs. These experiments suggest a role for Pitx2 in promoting looping of the linear heart and gut. (+info)Mrj encodes a DnaJ-related co-chaperone that is essential for murine placental development. (4/50418)
We have identified a novel gene in a gene trap screen that encodes a protein related to the DnaJ co-chaperone in E. coli. The gene, named Mrj (mammalian relative of DnaJ) was expressed throughout development in both the embryo and placenta. Within the placenta, expression was particularly high in trophoblast giant cells but moderate levels were also observed in trophoblast cells of the chorion at embryonic day 8.5, and later in the labyrinth which arises from the attachment of the chorion to the allantois (a process called chorioallantoic fusion). Insertion of the ROSAbetageo gene trap vector into the Mrj gene created a null allele. Homozygous Mrj mutants died at mid-gestation due to a failure of chorioallantoic fusion at embryonic day 8.5, which precluded formation of the mature placenta. At embryonic day 8.5, the chorion in mutants was morphologically normal and expressed the cell adhesion molecule beta4 integrin that is known to be required for chorioallantoic fusion. However, expression of the chorionic trophoblast-specific transcription factor genes Err2 and Gcm1 was significantly reduced. The mutants showed no abnormal phenotypes in other trophoblast cell types or in the embryo proper. This study indicates a previously unsuspected role for chaperone proteins in placental development and represents the first genetic analysis of DnaJ-related protein function in higher eukaryotes. Based on a survey of EST databases representing different mouse tissues and embryonic stages, there are 40 or more DnaJ-related genes in mammals. In addition to Mrj, at least two of these genes are also expressed in the developing mouse placenta. The specificity of the developmental defect in Mrj mutants suggests that each of these genes may have unique tissue and cellular activities. (+info)A Drosophila doublesex-related gene, terra, is involved in somitogenesis in vertebrates. (5/50418)
The Drosophila doublesex (dsx) gene encodes a transcription factor that mediates sex determination. We describe the characterization of a novel zebrafish zinc-finger gene, terra, which contains a DNA binding domain similar to that of the Drosophila dsx gene. However, unlike dsx, terra is transiently expressed in the presomitic mesoderm and newly formed somites. Expression of terra in presomitic mesoderm is restricted to cells that lack expression of MyoD. In vivo, terra expression is reduced by hedgehog but enhanced by BMP signals. Overexpression of terra induces rapid apoptosis both in vitro and in vivo, suggesting that a tight regulation of terra expression is required during embryogenesis. Terra has both human and mouse homologs and is specifically expressed in mouse somites. Taken together, our findings suggest that terra is a highly conserved protein that plays specific roles in early somitogenesis of vertebrates. (+info)Requirement of a novel gene, Xin, in cardiac morphogenesis. (6/50418)
A novel gene, Xin, from chick (cXin) and mouse (mXin) embryonic hearts, may be required for cardiac morphogenesis and looping. Both cloned cDNAs have a single open reading frame, encoding proteins with 2,562 and 1,677 amino acids for cXin and mXin, respectively. The derived amino acid sequences share 46% similarity. The overall domain structures of the predicted cXin and mXin proteins, including proline-rich regions, 16 amino acid repeats, DNA-binding domains, SH3-binding motifs and nuclear localization signals, are highly conserved. Northern blot analyses detect a single message of 8.9 and 5.8 kilo base (kb) from both cardiac and skeletal muscle of chick and mouse, respectively. In situ hybridization reveals that the cXin gene is specifically expressed in cardiac progenitor cells of chick embryos as early as stage 8, prior to heart tube formation. cXin continues to be expressed in the myocardium of developing hearts. By stage 15, cXin expression is also detected in the myotomes of developing somites. Immunofluorescence microscopy reveals that the mXin protein is colocalized with N-cadherin and connexin-43 in the intercalated discs of adult mouse hearts. Incubation of stage 6 chick embryos with cXin antisense oligonucleotides results in abnormal cardiac morphogenesis and an alteration of cardiac looping. The myocardium of the affected hearts becomes thickened and tends to form multiple invaginations into the heart cavity. This abnormal cellular process may account in part for the abnormal looping. cXin expression can be induced by bone morphogenetic protein (BMP) in explants of anterior medial mesoendoderm from stage 6 chick embryos, a tissue that is normally non-cardiogenic. This induction occurs following the BMP-mediated induction of two cardiac-restricted transcription factors, Nkx2.5 and MEF2C. Furthermore, either MEF2C or Nkx2.5 can transactivate a luciferase reporter driven by the mXin promoter in mouse fibroblasts. These results suggest that Xin may participate in a BMP-Nkx2.5-MEF2C pathway to control cardiac morphogenesis and looping. (+info)Mechanisms of GDF-5 action during skeletal development. (7/50418)
Mutations in GDF-5, a member of the TGF-beta superfamily, result in the autosomal recessive syndromes brachypod (bp) in mice and Hunter-Thompson and Grebe-type chondrodysplasias in humans. These syndromes are all characterised by the shortening of the appendicular skeleton and loss or abnormal development of some joints. To investigate how GDF-5 controls skeletogenesis, we overexpressed GDF-5 during chick limb development using the retrovirus, RCASBP. This resulted in up to a 37.5% increase in length of the skeletal elements, which was predominantly due to an increase in the number of chondrocytes. By injecting virus at different stages of development, we show that GDF-5 can increase both the size of the early cartilage condensation and the later developing skeletal element. Using in vitro micromass cultures as a model system to study the early steps of chondrogenesis, we show that GDF-5 increases chondrogenesis in a dose-dependent manner. We did not detect changes in proliferation. However, cell suspension cultures showed that GDF-5 might act at these stages by increasing cell adhesion, a critical determinant of early chondrogenesis. In contrast, pulse labelling experiments of GDF-5-infected limbs showed that at later stages of skeletal development GDF-5 can increase proliferation of chondrocytes. Thus, here we show two mechanisms of how GDF-5 may control different stages of skeletogenesis. Finally, our data show that levels of GDF-5 expression/activity are important in controlling the size of skeletal elements and provides a possible explanation for the variation in the severity of skeletal defects resulting from mutations in GDF-5. (+info)Regulation of body length and male tail ray pattern formation of Caenorhabditis elegans by a member of TGF-beta family. (8/50418)
We have identified a new member of the TGF-beta superfamily, CET-1, from Caenorhabditis elegans, which is expressed in the ventral nerve cord and other neurons. cet-1 null mutants have shortened bodies and male tail abnormal phenotype resembling sma mutants, suggesting cet-1, sma-2, sma-3 and sma-4 share a common pathway. Overexpression experiments demonstrated that cet-1 function requires wild-type sma genes. Interestingly, CET-1 appears to affect body length in a dose-dependent manner. Heterozygotes for cet-1 displayed body lengths ranging between null mutant and wild type, and overexpression of CET-1 in wild-type worms elongated body length close to lon mutants. In male sensory ray patterning, lack of cet-1 function results in ray fusions. Epistasis analysis revealed that mab-21 lies downstream and is negatively regulated by the cet-1/sma pathway in the male tail. Our results show that cet-1 controls diverse biological processes during C. elegans development probably through different target genes. (+info)Some common effects of chromosomal deletions include:
1. Genetic disorders: Chromosomal deletions can lead to a variety of genetic disorders, such as Down syndrome, which is caused by a deletion of a portion of chromosome 21. Other examples include Prader-Willi syndrome (deletion of chromosome 15), and Williams syndrome (deletion of chromosome 7).
2. Birth defects: Chromosomal deletions can increase the risk of birth defects, such as heart defects, cleft palate, and limb abnormalities.
3. Developmental delays: Children with chromosomal deletions may experience developmental delays, learning disabilities, and intellectual disability.
4. Increased cancer risk: Some chromosomal deletions can increase the risk of developing certain types of cancer, such as chronic myelogenous leukemia (CML) and breast cancer.
5. Reproductive problems: Chromosomal deletions can lead to reproductive problems, such as infertility or recurrent miscarriage.
Chromosomal deletions can be diagnosed through a variety of techniques, including karyotyping (examination of the chromosomes), fluorescence in situ hybridization (FISH), and microarray analysis. Treatment options for chromosomal deletions depend on the specific effects of the deletion and may include medication, surgery, or other forms of therapy.
There are several types of inborn errors of amino acid metabolism, including:
1. Phenylketonuria (PKU): This is the most common inborn error of amino acid metabolism and is caused by a deficiency of the enzyme phenylalanine hydroxylase. This enzyme is needed to break down the amino acid phenylalanine, which is found in many protein-containing foods. If phenylalanine is not properly broken down, it can build up in the blood and brain and cause serious health problems.
2. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
3. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
4. Arginase deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid arginine. Arginine is important for the body's production of nitric oxide, a compound that helps to relax blood vessels and improve blood flow.
5. Citrullinemia: This is a rare genetic disorder that affects the breakdown of the amino acid citrulline. Citrulline is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
6. Tyrosinemia: This is a rare genetic disorder that affects the breakdown of the amino acid tyrosine. Tyrosine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
7. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
8. PKU (phenylketonuria): This is a rare genetic disorder that affects the breakdown of the amino acid phenylalanine. Phenylalanine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
9. Methionine adenosyltransferase (MAT) deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
10. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid homocysteine. Homocysteine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
It is important to note that these disorders are rare and affect a small percentage of the population. However, they can be serious and potentially life-threatening, so it is important to be aware of them and seek medical attention if symptoms persist or worsen over time.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.
Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).
Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
https://www.medicinenet.com › Medical Dictionary › G
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Definition & Facts | Britannica
https://www.britannica.com › science › Genetic-tr...
Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.
Translocation, Genetic | health Encyclopedia - UPMC
https://www.upmc.com › health-library › gene...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Genetics Home Reference - NIH
https://ghr.nlm.nih.gov › condition › ge...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.
Hartnup disease is a rare genetic disorder that affects the body's ability to absorb vitamin B12 (cobalamin) and other nutrients. It is caused by a mutation in the HCN1 gene, which codes for a protein involved in the transport of cobalamin into the cells.
Symptoms of Hartnup Disease:
The symptoms of Hartnup disease can vary in severity and may include:
* Fatigue
* Weakness
* Pale skin
* Shortness of breath
* Dizziness
* Headaches
* Numbness or tingling in the hands and feet
* Seizures
* Poor appetite
* Diarrhea
Complications of Hartnup Disease:
If left untreated, Hartnup disease can lead to complications such as:
* Anemia (low red blood cell count)
* Nerve damage
* Skin problems
* Eye problems
* Hearing loss
* Increased risk of infections
Treatment of Hartnup Disease:
The treatment of Hartnup disease typically involves a combination of dietary changes and supplements. Patients with the condition may need to follow a strict diet that includes foods high in vitamin B12, such as meat, fish, and dairy products. They may also need to take supplements to ensure they are getting enough of this important nutrient. In some cases, medication may be prescribed to help manage symptoms.
Prognosis of Hartnup Disease:
The prognosis for Hartnup disease is generally good if the condition is diagnosed and treated early. With proper management, most patients with Hartnup disease can lead active and healthy lives. However, if left untreated, the condition can have serious complications that can be difficult to reverse.
Inheritance Pattern of Hartnup Disease:
Hartnup disease is an autosomal recessive disorder, which means that a person must inherit two copies of the mutated HCN1 gene (one from each parent) in order to develop the condition. If a person inherits only one copy of the mutated gene, they will be a carrier of the condition but are unlikely to develop symptoms themselves. Carriers of Hartnup disease can pass the mutated gene on to their children, who have a 25% chance of inheriting two copies of the gene and developing the condition.
Prevention of Hartnup Disease:
There is no known prevention for Hartnup disease. However, if a person knows they are a carrier of the condition, they can work with their healthcare provider to ensure they are getting enough vitamin B12 and monitoring their diet to prevent any complications.
In conclusion, Hartnup disease is a rare genetic disorder that affects the absorption of vitamin B12 in the small intestine. It can cause a range of symptoms, including diarrhea, abdominal pain, and fatigue. Treatment typically involves a combination of dietary changes and supplements, and early diagnosis and management can lead to a good prognosis. However, if left untreated, the condition can have serious complications. If you suspect you or someone you know may be experiencing symptoms of Hartnup disease, it is important to speak with a healthcare provider for proper diagnosis and treatment.
The ABCD1 gene plays a critical role in the energy metabolism of the nervous system, and mutations in this gene can disrupt normal nerve cell function. As a result, Kearns-Sayre Syndrome is considered an example of a mitochondrial disorder - a group of diseases caused by defects in the mitochondria, the energy-producing structures within cells.
Kearns-Sayre Syndrome is extremely rare and affects approximately one in 1 million people worldwide. It is usually inherited in an autosomal recessive pattern, meaning that a child must inherit two copies of the mutated gene - one from each parent - to develop the syndrome. However, some cases may also be caused by spontaneous genetic mutations.
There is currently no cure for Kearns-Sayre Syndrome, but various treatments are available to manage its symptoms and slow its progression. These may include medications to control seizures, physical therapy to maintain muscle strength and function, and supportive care to address any associated complications. In some cases, bone marrow transplantation or enzyme replacement therapy may also be considered as potential treatment options.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Cystinuria is caused by mutations in the SLC7A9 gene, which codes for a protein involved in the transport of cystine across the brush border membrane of renal tubular cells. The disorder is inherited in an autosomal recessive pattern, meaning that affected individuals must inherit two copies of the mutated gene (one from each parent) to develop symptoms.
There is no cure for cystinuria, but various treatments can help manage its symptoms. These may include medications to reduce the acidity of the urine and prevent infection, as well as surgical procedures to remove stones or repair damaged kidneys. In some cases, a kidney transplant may be necessary.
It's important for individuals with cystinuria to drink plenty of water and maintain good hydration to help flush out the urinary tract and prevent stone formation. They should also avoid certain foods that may increase the risk of stone formation, such as oxalate-rich foods like spinach and rhubarb.
Overall, while there is no cure for cystinuria, with proper management and care, individuals with this disorder can lead relatively normal lives and minimize the complications associated with it.
There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
Inversions are classified based on their location along the chromosome:
* Interstitial inversion: A segment of DNA is reversed within a larger gene or group of genes.
* Pericentric inversion: A segment of DNA is reversed near the centromere, the region of the chromosome where the sister chromatids are most closely attached.
Chromosome inversions can be detected through cytogenetic analysis, which allows visualization of the chromosomes and their structure. They can also be identified using molecular genetic techniques such as PCR (polymerase chain reaction) or array comparative genomic hybridization (aCGH).
Chromosome inversions are relatively rare in the general population, but they have been associated with various developmental disorders and an increased risk of certain diseases. For example, individuals with an inversion on chromosome 8p have an increased risk of developing cancer, while those with an inversion on chromosome 9q have a higher risk of developing neurological disorders.
Inversions can be inherited from one or both parents, and they can also occur spontaneously as a result of errors during DNA replication or repair. In some cases, inversions may be associated with other genetic abnormalities, such as translocations or deletions.
Overall, chromosome inversions are an important aspect of human genetics and can provide valuable insights into the mechanisms underlying developmental disorders and disease susceptibility.
Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
There are several types of PKU, including classic PKU, mild PKU, and hyperphenylalaninemia (HPA). Classic PKU is the most severe form of the disorder and is characterized by a complete deficiency of the enzyme phenylalanine hydroxylase (PAH), which is necessary for the breakdown of Phe. Mild PKU is characterized by a partial deficiency of PAH, while HPA is caused by a variety of other genetic defects that affect the breakdown of Phe.
Symptoms of PKU can vary depending on the severity of the disorder, but may include developmental delays, intellectual disability, seizures, and behavioral problems. If left untreated, PKU can lead to serious health complications such as brain damage, seizures, and even death.
The primary treatment for PKU is a strict diet that limits the intake of Phe. This typically involves avoiding foods that are high in Phe, such as meat, fish, eggs, and dairy products, and consuming specialized medical foods that are low in Phe. In some cases, medication may also be prescribed to help manage symptoms.
PKU is an autosomal recessive disorder, which means that it is inherited in an unusual way. Both parents must carry the genetic mutation that causes PKU, and each child has a 25% chance of inheriting the disorder. PKU can be diagnosed through newborn screening, which is typically performed soon after birth. Early diagnosis and treatment can help prevent or minimize the symptoms of PKU and improve quality of life for individuals with the disorder.
Also known as: aminoacyl-tRNA synthetase deficiency, aminoacyl-tRNA synthetase/tRNA synthetase deficiency, and amino acid transporter defects.
There are several types of melanoma, including:
1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.
The risk factors for developing melanoma include:
1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma
The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:
1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole
If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.
In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.
Piscivorin
Fructose 1,6-bisphosphatase
GroEL
MTA2
Chemokine
Clostridium difficile toxin A
Subtilase
YARS
Interleukin-1 family
Triptan
KLK1
5-HT1E receptor
Type three secretion system
Rho-associated protein kinase
Glycodelin
Fibroblast growth factor
Bone growth factor
Chlorotoxin
Bacillus anthracis
ALPI
ATP2A1
Sequence homology
Eukaryotic translation elongation factor 1 alpha 1
Mucorpepsin
International Union of Pure and Applied Chemistry
Protein 4.2
Carnitine palmitoyltransferase II deficiency
Serine dehydratase
CKAP2
Interferon alpha-1
Proto-oncogene tyrosine-protein kinase Src
TENM3
GNLY
HSPA1B
Thyroxine-binding globulin
Complementarity plot
Thromboxane-A synthase
Plasma membrane monoamine transporter
LDL receptor
Sigma-1 receptor
CAFASP
Structural genomics
Ubiquitin-like protein
Pyrobaculum
N-glycosyltransferase
Haemagglutination activity domain
SPTAN1
Alpha-lytic endopeptidase
NE-tag
Collagen, type IV, alpha 2
DNA-PKcs
Dihydrolipoamide dehydrogenase
Cangitoxin
Index of biochemistry articles
Parallel evolution
Nuclear receptor
Alkaline phosphatase
Coronin
Telomeric repeat-binding factor 2
Scarlet fever
The Candida albicans pescadillo homolog is required for normal hypha-to-yeast morphogenesis and yeast proliferation
Hepatitis E Virus Genotype 3 in Humans and Swine, Bolivia - Volume 17, Number 8-August 2011 - Emerging Infectious Diseases...
The Molecular Basis of Life - Birkbeck, University of London
2019-nCov Gene Sequence breakdown
Nitai P Bhattacharyya
Amyloidosis: Definition of Amyloid and Amyloidosis, Classification Systems, Systemic Amyloidoses
Comparative Analysis of SWIRM Domain-Containing Proteins in Plants
Volume 19, Number 12, décembre 2003 - M/S : médecine sciences - Érudit
SMART: WD40 domain annotation
IJMS | Free Full-Text | Recent Developments in Peptide-Based Nucleic Acid Delivery
Variant Annotation Integrator
An integrated metagenomic and metabolite profiling study of hydrocarbon biodegradation and corrosion in navy ships | npj...
Mapping of Structure-Function Peptide Sites on the Human Alpha-fetoprotein Amino Acid Sequence
SERINC1 Antibody - Cat. No. 59-217 | ProSci
Serum amyloid A is a retinol binding protein that transports retinol during bacterial infection | eLife
Variant Annotation Integrator
Analysis of genetic mutations in the 7a7b open reading frame of coronavirus of cheetahs (Acinonyx jubatus) in: American Journal...
Prediction of subcellular location of apoptosis proteins by incorporating PsePSSM and DCCA coefficient based on LFDA...
The picture gets more complex: ANO2 + GlialCam + CRYAB - This Is MS Multiple Sclerosis Knowledge & Support Community
Variant Annotation Integrator
DeCS
Characterization and production of amylovorin L471, a bacteriocin purified from Lactobacillus amylovorus DCE 471 by a novel...
Thyroid hormone-interacting cell and plasma proteins share a common motif
Frontiers | Characterization and Genome Structure of Virulent Phage EspM4VN to Control Enterobacter sp. M4 Isolated From Plant...
Characterization of Genes and Proteins Involved in Excision Repair of Human Cells | Journal of Cell Science | The Company of...
US Patent for Compositions and methods for the inhibition of membrane fusion by paramyxoviruses Patent (Patent # 7,666,431...
Development and validation of a house finch interleukin-1β (HfIL-1β) ELISA system | BMC Veterinary Research | Full Text
The RAD2 gene of Saccharomyces cerevisiae: nucleotide sequence and transcript mapping<...
Plus it
Residues6
- The computational sequence-profile analysis indicates that the typical SWIRM domain consists of 85 amino acid residues and forms a compact helix-turn-helix (HTH)-related structure [ 12 ]. (hindawi.com)
- The latter represent an assortment of fairly unrelated sequences essentially characterised by a high content of basic amino acids and a length of 10-30 residues. (mdpi.com)
- We now demonstrate further cross-reactivity between EBNA1 amino acids 402 to 406 and CRYAB amino acids 11 to 15 , with core sequence homology mapped to identical RRPFF residues within these fragments. (thisisms.com)
- While many proteins contain this core amino acid RRPFF motif, amino acid residues that flank this sequence and are unique to CRYAB are also necessary for antibody binding. (thisisms.com)
- N-terminal amino acid sequencing identified 35 amino acid residues as being identical to the N-terminal sequence of lactobin A, a bacteriocin from another L. amylovorus strain. (microbiologyresearch.org)
- 33-50% of sequences) groups of residues. (imrpress.com)
Proteins8
- Predicted to be a 44-amino-acid, highly hydrophobic protein with no identified sequence homology to other viral or cellular proteins. (godlikeproductions.com)
- The specificity of the proteins is determined by the sequences outside the repeats themselves. (embl.de)
- We chose proteins that include amino and carboxyl extensions as well as proteins that are made up entirely of WD-repeats. (embl.de)
- The atlas further shows AFP as a protein consisting of multiple peptide-cassettes consisting of amino acid (AA) sequence stretches matched to peptide segments on prohormones and biological response modifier proteins. (atlasgeneticsoncology.org)
- The AFP molecule is also viewed as a carrier/transport protein based on AA sequence comparison of various proteins that bind hydrophobic ligands and heavy metals similar to AFP binding of such components. (atlasgeneticsoncology.org)
- AFP AA sequences are further presented as peptide identification sites for growth factors, receptors, cytoskeletal proteins, and chemokines. (atlasgeneticsoncology.org)
- Sequence analysis of full-length cDNA copies of the two ERCC-1 mRNAs revealed open reading frames for proteins of 297 and 273 amino acids, respectively. (biologists.com)
- These types of RNA help assemble protein building blocks (amino acids) into functioning proteins. (medlineplus.gov)
Motifs3
- WD-40 repeats (also known as WD or beta-transducin repeats) are short ~40 amino acid motifs, often terminating in a Trp-Asp (W-D) dipeptide. (embl.de)
- An analysis of transcription factors, tumor suppressors, and AA-rich motifs follows, interfaced with dimerization and nuclear localization sequence matches identified on the AFP molecule. (atlasgeneticsoncology.org)
- A closing discussion summarizes the multiple and varied motifs of peptide sequences matched to AAs on each of AFP's three domains. (atlasgeneticsoncology.org)
Peptides2
- CPPs are capable of mediating the cellular uptake of hydrophilic macromolecules like peptides and nucleic acids (e.g. siRNAs, aptamers and antisense-oligonucleotides), which are internalised by cells at a very low rate when applied alone. (mdpi.com)
- The amino acid sequence of amylovorin L471 shared significant homology with lactacin X, one of the two bactericidal peptides produced by Lactobacillus johnsonii VPI11088 . (microbiologyresearch.org)
GENOMIC2
- The Human Genome Variation Society (HGVS) has established a sequence variant nomenclature , an international standard used to report variation in genomic, transcript and protein sequences. (ucsc.edu)
- There are significant structural features in the viral genomic RNA that could, by themselves, explain the retention of the ORF10 nucleotide sequences without the need for a functional protein product. (bvsalud.org)
Nucleic acid1
- Despite the fact that non-viral nucleic acid delivery systems are generally considered to be less efficient than viral vectors, they have gained much interest in recent years due to their superior safety profile compared to their viral counterpart. (mdpi.com)
Antibodies1
- showed serum antibodies from MS patients are cross-reactive between amino acids 411-440 of the viral protein EBV nuclear antigen 1 (EBNA-1) and the human chloride-channel protein, anoctamin 2 (ANO2), which is associated with electrical conduction in axons (11). (thisisms.com)
Viral2
- Sequencing of viral RNA in the lungs of hamsters infected with ORF10KO virus revealed that this virus frequently reverts to WT. (bvsalud.org)
- Viral sequences, that passed genome quality control criteria, from subjects who received molnupiravir (n=59) or a placebo (n=65) were analysed by high-throughput amplicon sequencing. (bvsalud.org)
Hydrophobic1
- Unlike ALB, high concentrations of hydrophobic ligands (i.e., fatty acids, estrogens) have been reported to induce multiple conformational transition forms, which are reversible, in the tertiary structure of HAFP (see ref. (atlasgeneticsoncology.org)
Nuclear2
- We hypothesized that a thyroid hormone (TH)-binding consensus sequence, which is shared by human and animal TH plasma carriers (THPC), might also be shared by cell surface TH transporters (CMTTH) and TH nuclear receptors (THR). (imrpress.com)
- On the basis of homology with functional protein domains a tentative nuclear location signal, DNA binding domain and ADP-ribosylation site could be identified in the ERCC-1 aa sequence. (biologists.com)
Protein sequences2
- Firstly, the protein sequences are extracted by combining pseudo-position specific scoring matrix (PsePSSM) and detrended cross-correlation analysis coefficient (DCCA coefficient), then the extracted feature information is reduced dimensionality by LFDA (local Fisher discriminant analysis). (biomedcentral.com)
- As for protein subcellular localization prediction methods, we found that the research focuses on the following two aspects: (1) Feature extraction of protein sequences. (biomedcentral.com)
Similarity1
- The degree of similarity between sequences of amino acids. (bvsalud.org)
Ligands1
- This sequence contains amino acids common to the ligands of G protein-coupled receptors, but has no known homology. (atsbio.com)
Significant1
- Significant amino acid sequence homology was found between portions of the putative ERCC-1 product and the protein encoded by the yeast excision-repair gene RAD10 . (biologists.com)
Apoptosis2
- Emphasis is further placed upon homeodomain and apoptosis AA sequence identities given that AFP serves as a fetal, phase-specific protein throughout embryogenesis, histogenesis, and organogenesis. (atlasgeneticsoncology.org)
- Zhou and Doctor [ 36 ] constructed 98 protein apoptosis protein dataset, using the amino acid composition and covariance discriminant method, the overall prediction accuracy reached 72.5% by jackknife test. (biomedcentral.com)
Rabbits1
- This SERINC1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 353-379 amino acids from the C-terminal region of human SERINC1. (prosci-inc.com)
Genome1
- To explore this question further we made two recombinant viruses, firstly a control virus (WT) based on the genome sequence of the original Wuhan isolate and with the inclusion of the early D614G mutation in the Spike protein. (bvsalud.org)
Functional1
- Our data suggests that the retention of a functional ORF10 sequence is highly desirable for SARS-CoV-2 infection of hamsters and affects the virus's ability to propagate in the lower respiratory tract. (bvsalud.org)
Retinoic1
- However, treating the cells with retinol or the molecule it is broken down into-called retinoic acid-caused more SAAs to be made. (elifesciences.org)
Gene1
- Numbers along rows represent predicted amino acid position within the 7a7b gene product. (avma.org)
RNAs1
- Fusion sequences characteristic of defective RNAs were identified that could be linked between patients. (bvsalud.org)
Antigen1
- In addition, EBNA1 amino acids 411 to 426 and myelin basic protein cross-reactivity has been demonstrated in experimental autoimmune encephalomyelitis (EAE) (36), and EBNA1-specific T cells have been shown to react to a mixed myelin antigen pool (33). (thisisms.com)
Composition1
- NPAA domain of human HYPK has unique amino acid composition preferring glutamic acid and happens to be more stable from a conformational point of view having higher content of 𝛼-helices than the rest. (ias.ac.in)
Analysis1
- Amino acid sequence analysis revealed 105 orthologs of human HYPK from plants, lower invertebrates to mammals. (ias.ac.in)
Antibody1
- Because recombinant antibody production involves sequencing the antibody light and heavy chains, it is a highly controlled and reliable process. (cellsignal.com)
Consensus2
- We generated the consensus for CMTTH or THR from 8,691 or 624 sequences. (imrpress.com)
- The sequence data confirmed that the dominant consensus genomes shared very close homology. (bvsalud.org)
Viruses1
- Growth competition experiments were used whereby the two viruses were mixed, passaged in either VTN or A549-AT cells and the resulting output virus was sequenced. (bvsalud.org)
Genetic1
- In effort to better understand how 2019-nCoV affects the infected I pulled one of the available genetic sequences and started researching each component. (godlikeproductions.com)
Matches1
- 13 Amino acid matches to reference strain are indicated by a dash. (avma.org)
Virus2
Human2
- Human HYPK (Huntingtin Yeast-two-hybrid Protein K) is an intrinsically unstructured chaperone-like protein with no sequence homology to known chaperones. (ias.ac.in)
- Based on the domain architectures and the amino acid sequence homology, the SWIRM domains can be classified into three main types: Swi3/MYSM1 (human MYb-like, Swirm, and Mpn domain-containing protein-1), LSD1 (Lysine-specific demethylase 1), and Ada2 (Adenosine deaminase isoenzymes 2) types [ 13 ]. (hindawi.com)
Article1
- Cet article illustre ces aspects en prenant pour exemples deux maladies héréditaires, la myopathie de Duchenne et la chorée de Huntington. (erudit.org)
Alpha1
- The non-WD-repeat amino terminal alpha helix of G beta does not inhibit folding because G beta does not fold even when this region is removed. (embl.de)
Production1
- Characterization and production of amylovorin L471, a bacteriocin purified from Lactobacillus amylovorus DCE 471 by a novel three-step methodThe GenBank/EMBL/DDBJ accession number for the sequence reported in this paper is P81927. (microbiologyresearch.org)
Structure1
- Native or wild-type quaternary protein structure is usually born from a single translated protein sequence with one ordered conformation with downstream protein interactions. (medscape.com)
Understand1
- [ 4 ] It is also important to understand that the same polypeptide sequence can produce many different patterns of interresidue or intraresidue interactions. (medscape.com)