Pathways

Josamycin is a macrolide antibiotic from Streptomyces narbonensis. The drug has antimicrobial activity against a wide spectrum of pathogens and used for the treatment of bacterial infections. Josamycin targets the protein synthesis machinery in the bacterial cytoplasm to inhibit protein synthesis and prevent bacterial growth. Josamycin enters through the bacterial cell membrane through a transporter and binds to the bacterial ribosome. The bacterial ribosome consists of two subunits: the 50s and the 30s subunit. Josamycin binds to the 50s subunit and prevents translocation of the tRNA along the A, P and E sites of the ribosome. Translocation of amino acids from the acceptor site (A site) to the donor site (P site) is prevented and as a result, protein synthesis is halted. The bacterial cells are unable to generate proteins necessary for growth and duplication, therefore, growth of the bacteria is inhibited. This action is mainly bacteriostatic, but can also be bactericidal at high concentrations. Macrolides tend to accumulate within leukocytes, and are therefore actually transported into the site of infection. Side effects from taking josamycin may include abdominal pain, nausea, vomiting, diarrhea and skin rashes.

Josamycin is a macrolide antibiotic that is synthesized from Streptomyces narbonensis which can against various pathogens. Josamycin inhibits protein biosynthesis of bacteria by binding to ribosomal 50S subunit reversibly, which lead to inhibition of translocation of peptidyl tRNA. This action is mainly bacteriostatic, but can also be bactericidal in high concentrations. Macrolides can be accumulated within leukocytes, and transport into infection site later on.

Joubert syndrome is a condition in which brain development is not completed as it should be, including the lack or underdevelopment of the part of the brain that regulates balance and coordination and an abnormal brain stem. The symptoms affect a variety of body parts in the patient, including apnea, ataxia brought on by hypotonia, abnormal eye movements and intellectual disability. Many different gene mutations are responsible for Joubert syndrome, all of the proteins created from these genes affecting the cilia that are found on the cell surface. It can be confirmed through its hallmark molar tooth imprint that shows up on brain scans of the patient, a visualization of the malformed brain stem and cerebellar vermis.

Joubert syndrome is a condition in which brain development is not completed as it should be, including the lack or underdevelopment of the part of the brain that regulates balance and coordination and an abnormal brain stem. The symptoms affect a variety of body parts in the patient, including apnea, ataxia brought on by hypotonia, abnormal eye movements and intellectual disability. Many different gene mutations are responsible for Joubert syndrome, all of the proteins created from these genes affecting the cilia that are found on the cell surface. It can be confirmed through its hallmark molar tooth imprint that shows up on brain scans of the patient, a visualization of the malformed brain stem and cerebellar vermis.

Joubert syndrome is a condition in which brain development is not completed as it should be, including the lack or underdevelopment of the part of the brain that regulates balance and coordination and an abnormal brain stem. The symptoms affect a variety of body parts in the patient, including apnea, ataxia brought on by hypotonia, abnormal eye movements and intellectual disability. Many different gene mutations are responsible for Joubert syndrome, all of the proteins created from these genes affecting the cilia that are found on the cell surface. It can be confirmed through its hallmark molar tooth imprint that shows up on brain scans of the patient, a visualization of the malformed brain stem and cerebellar vermis.

Joubert syndrome is a condition in which brain development is not completed as it should be, including the lack or underdevelopment of the part of the brain that regulates balance and coordination and an abnormal brain stem. The symptoms affect a variety of body parts in the patient, including apnea, ataxia brought on by hypotonia, abnormal eye movements and intellectual disability. Many different gene mutations are responsible for Joubert syndrome, all of the proteins created from these genes affecting the cilia that are found on the cell surface. It can be confirmed through its hallmark molar tooth imprint that shows up on brain scans of the patient, a visualization of the malformed brain stem and cerebellar vermis.

Juvenile hormones in insects are important for their growth before their adulthood, preventing metamorphosis if they undergo one. In Drosophila, only juvenile hormone III has been identified, while others exist in butterflies and moths. Synthesis of various forms of juvenile hormone III (JH III) start with farnesyl diphosphate interacting with an uncharacterized phosphatase protein, forming farnesol. Farnesol then interacts with NADP+ dependent farensol dehydrogenase, which removes a hydrogen ion from the hydroxyl group in order to form farnesal. Farnesal then enters the mitochondria and interacts with another uncharacterized aldehyde dehydrogenase which allows it to form farnesoic acid. Farnesoic acid can then interact with an unknown protein, similar to farnesoate epoxidase in Bombyx mori, in order to form juvenile hormone III acid (JH III acid). JH III acid can then interact with epoxide hydrolase in the membrane of the endoplasmic reticulum, forming the final product of this pathway, juvenile hormone III acid diol (JH III acid diol). It can also interact with juvenile hormone acid O-methyltransferase in order to form JH III, which is used in another set of reactions in this pathway. If farnesoic acid does not interact with the unknown protein, it may interact with juvenile hormone acid O-methyltransferase to form methyl farnesoate. Methyl farnesoate can then interact with a different unknown protein similar, to methyl farnesoate epoxidase in Diploptera punctata, in order to form JH III. In the mitochondria, JH III can interact with carboxylic ester hydrolase in order to form JH III acid, which then can form the final product, or form JH III again. Alternately, JH III can interact with epoxide hydrolase in the membrane of the endoplasmic reticulum, forming juvenile hormone III diol. This product then interacts with carboxylic ester hydrolase in the mitochondria, forming JH III acid diol, again, the end product of this pathway.