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Updated: Jul 8, 2026

Why Quantification Matters: Characterization of Phenotypes at the Drosophila Larval Neuromuscular Junction
10:41

Why Quantification Matters: Characterization of Phenotypes at the Drosophila Larval Neuromuscular Junction

Published on: May 12, 2016

遺伝性性 paraplegia で欠陥がある m-AAA プロテアゼは,ミトコンドリアのリボソーム組立を制御する

Mark Nolden1, Sarah Ehses, Mirko Koppen

  • 1Institute for Genetics and Center for Molecular Medicine, University of Cologne, 50674 Cologne, Germany.

Cell
|October 22, 2005
PubMed
まとめ

AAAプロテアゼは,リボソーム組立に不可欠なMrpL32タンパク質を処理することによって,ミトコンドリアのタンパク質合成を調節する. この発見は,ミトコンドリアの欠陥と遺伝性性パラペルジアのメカニズムを説明します.

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CD Spectroscopy to Study DNA-Protein Interactions06:48

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures08:41

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures

Published on: December 27, 2024

関連する概念動画

Mismatch Repair01:36

Mismatch Repair

Overview
Nucleosome Remodeling02:54

Nucleosome Remodeling

Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
Biosynthesis of Nucleic Acids01:28

Biosynthesis of Nucleic Acids

Nucleic acid biosynthesis is a fundamental biochemical process that produces the purine and pyrimidine nucleotides essential for DNA and RNA synthesis. This pathway maintains a balanced nucleotide pool, preventing imbalances that could jeopardize genetic integrity and cellular function. Given the crucial role of nucleotides, their synthesis is tightly regulated to ensure proper cellular homeostasis.Purine BiosynthesisThe biosynthesis of purine nucleotides begins with ribose-5-phosphate, a...