DEFISIENSI ENZIM G6PD PDF

Patofisiologi Defisiensi Enzim G6PD. NADPH yang dihasilkan dalam lintasan pentose fosfat oleh aktifitas G6PD berperan dalam eritrosit untuk mereduksi. Defisiensi Enzim Glukosa 6 Fosfat Dehidrogenase (G6PD) – Download as Powerpoint Presentation .ppt /.pptx), PDF File .pdf), Text File .txt) or view. PERBANDINGAN KADAR BILIRUBIN NEONATUS DENGAN DAN TANPA DEFISIENSI GLUCOSEPHOSPHATE DEHYDROGENASE, INFEKSI DAN TIDAK.

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All green dashes represent distances less than 3.

Glucose-6-phosphate dehydrogenase

The oxygen atoms of crystallographic water molecules are shown as red spheres. With access to crystal structures, some scientists have tried to defiwiensi the structures of other mutants. Comptes Rendus Biologies in French.

Views Read Edit View history. Phosphopentose isomerase Phosphopentose epimerase Transketolase Transaldolase. The proline at position is thought to play a crucial role in positioning Lys correctly with respect to the substrate, G6P.

Glucosephosphate dehydrogenase – Wikipedia

There are about nine variants of G6PD deficiency. To do this, he will require a list of the medications the patient have been taking, food that he consumed prior to enzmi the symptoms, and chemicals that he may have come in contact. Goldman L, Ausiello D, eds. The K acetylated G6PD is incapable of forming active dimers enzom displays a complete loss of activity.

When a patient is diagnosed with G6PD deficiency, the doctor will analyze what triggered the condition. The patient will also be prescribed with medications that help induce the production of red blood cells.

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What is G6PD Deficiency: Symptoms, Causes, Diagnosis, and Treatment

The conserved 9-peptide sequence of G6PD is show in cyan. The body is usually able to produce a sufficient amount of red blood cells to replace those that die naturally, but with cells dying sooner than expected, the body is unable to keep up with the demand. Retrieved from ” https: As one of the largest medical tourism companies in the region, we are able to secure and share the critical information that is most linked to quality and cost of care.

All green dashes represent distances less than 4. Clinically, an X-linked genetic deficiency of G6PD predisposes a person to non-immune hemolytic anemia.

Since G6PD is an inherited disorder, one of the common concerns of people diagnosed with the condition is the chances of defisiesi passing on the disorder to their children. At DocDoc, we believe that it’s unfair for a doctor in private practice to discriminate against someone because they are flying overseas for care.

These cells are produced in the bone marrow and have a lifespan of about days. The structural site has been shown to be important for maintaining the long term stability of the enzyme.

In particular, there is a strong network of hydrogen bonding with electrostatic charges being diffused across multiple atoms through hydrogen bonding with 4 water molecules see figure.

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Hoffman R, Benz Jr. In the two crystal structures of normal human G6P, Pro is seen exclusively in the cis confirmation, while in the crystal structure of one disease causing mutant variant Canton RLPro is seen almost exclusively in the trans confirmation.

D-lactate dehydrogenase cytochrome D-lactate dehydrogenase cytochrome c Mannitol dehydrogenase cytochrome. G6PD is generally found as a dimer of two identical monomers see main thumbnail. This enzyme participates in the pentose phosphate pathway see imagea metabolic pathway that supplies reducing energy to cells such as erythrocytes by maintaining the level of the co-enzyme nicotinamide adenine dinucleotide phosphate NADPH.

G6PD is remarkable for its genetic diversity. This page was last edited on 28 Julyat EC number Enzyme superfamily Enzyme family List of enzymes. Every organ in the body needs a steady supply of oxygen-rich blood to function properly.

Hemolysis can also occur due to other factors, such as certain types of medications or damage to an artificial heart. Hydrogen bonding and electrostatic interaction network green. G6PD deficiency is a genetic disorder of the red blood cells, which is usually passed down by the mother.