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IgorLugansk [536]
3 years ago
5

In the Calvin cycle more atp than nadph is used how is this difference made up

Biology
1 answer:
Veseljchak [2.6K]3 years ago
8 0

Answer:

Explanation:

The detailed description of photosynthesis is that chlorophyll a becomes oxidized chlorophyll a after being irradiated, and the water in the thylakoid is oxidized by oxidized chlorophyll a to form oxygen and hydrogen ions, and hydrogen ions pass through the class. The ATP synthase on the capsule membrane passes through the membrane into the chloroplast matrix, where it provides a certain chemical potential (ie, an energy produced from a high concentration to a low concentration), and then ADP and Pi on the membrane. Will get energy to form ATP; and NADPH+ is the front chlorophyll a is oxidized by light to release high-energy electrons e, e will be transferred to NADP+ (oxidized coenzyme II), the photolysis of the front water does not produce hydrogen ions? This led to the combination of NADP and H+, which became NADPH.

Next, their use, in front of the photoreaction, in the dark reaction, CO2 will react with the five-carbon compound in the chloroplast matrix, fixed to the formation of a three-carbon compound (one C in CO2, five C in five-carbon compound, Two three-carbon compounds are formed, and then ATP and NADPH supply hydrogen, respectively, and then return to ADP+Pi and NADP+, and the reduced three-carbon compound becomes organic (mostly sugar) and becomes The five-carbon compound will react with CO2 again, which is the Calvin cycle.

<em>Genetic mutation is an important factor that contributes to the pathogenesis and development of Alzheimer’s disease (AD). The genetic factors studied include the dominant mutations of genes encoding amyloid-β precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2). Additionally, more and more genes have been found to be potentially associated with AD, such as apolipoprotein E (APOE), glycogen synthase kinase 3 beta (GSK3B), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A), and Tau. Although many studies on the treatment of AD have not been successful, gene therapy is still considered as a potential way against AD, and some gene-therapy-based therapeutics have entered the clinical trial stage. Existing strategies for gene therapy against AD include gene inactivation, genetic modification, and immunoregulation, etc.</em>

<em>https://www.creativebiomart.net/alzheimacy/therapeutics/gene-therapy/</em>

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