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Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondria01:37

Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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The Inner Mitochondrial Membrane01:28

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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Mitochondria Profoundly Influence Apolipoprotein E Biology.

Alexander P Gabrielli1,2, Ian Weidling1,2, Amol Ranjan1

  • 1University of Kansas Alzheimer's Disease Research Center, Kansas City, KS, USA.

Journal of Alzheimer'S Disease : JAD
|February 13, 2023
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Mitochondrial dysfunction significantly increases apolipoprotein E (APOE) expression in neuronal cells. This finding reveals a link between mitochondrial health and APOE, a key factor in Alzheimer

Keywords:
APOEAlzheimer’s diseaseapolipoprotein Emitochondriamitochondrial DNA

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Mitochondria play a role in Alzheimer's disease (AD) pathogenesis.
  • The influence of mitochondrial dysfunction on apolipoprotein E (APOE) remains largely unexplored.
  • APOE is a critical genetic risk factor for AD.

Purpose of the Study:

  • To investigate the impact of mitochondrial dysfunction on APOE gene and protein expression.
  • To elucidate the molecular mechanisms by which mitochondria influence APOE in neuronal cells.

Main Methods:

  • Utilized human SH-SY5Y neuronal cells with induced mitochondrial dysfunction (mtDNA depletion, toxin exposure).
  • Quantified APOE mRNA and apoE protein levels (intracellular and secreted).
  • Assessed the role of transcription factors (C/EBPα, Nrf2) and signaling pathways (JNK, ERK).

Main Results:

  • Mitochondrial dysfunction led to a substantial increase in APOE mRNA (65-fold) and apoE protein (8-fold increase in secreted).
  • Various forms of mitochondrial impairment consistently elevated APOE mRNA.
  • Knockdown of C/EBPα and Nrf2, and modulation of JNK/ERK activity, affected APOE mRNA levels in dysfunctional cells.

Conclusions:

  • Primary mitochondrial dysfunction activates APOE expression in neuronal cells via transcription factors and stress pathways.
  • Mitochondrial biology directly influences APOE gene and protein, relevant to Alzheimer's disease.
  • Establishes a novel connection between mitochondrial integrity and APOE regulation in the context of AD.