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Related Concept Videos

Proteomics01:33

Proteomics

A proteome is the entire set of proteins that a cell type produces. We can study proteomes using the knowledge of genomes because genes code for mRNAs, and the mRNAs encode proteins. Although mRNA analysis is a step in the right direction, not all mRNAs are translated into proteins.
Proteomics is the study of proteomes' function. It involves the large-scale systematic study of the proteome to denote the protein complement expressed by a genome. Scientist Mark Wilkins coined the term proteomics...
Ribosome Profiling02:24

Ribosome Profiling

Ribosome profiling or ribo-sequencing is a deep sequencing technique that produces a snapshot of active translation in a cell. It selectively sequences the mRNAs protected by ribosomes to get an insight into a cell’s translation landscape at any given point in time.
Applications of ribosome profiling
Ribosome profiling has many applications, including in vivo monitoring of translation inside a particular organ or tissue type and quantifying new protein synthesis levels.
The technique helps...

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Quantitative Proteomics Workflow using Multiple Reaction Monitoring Based Detection of Proteins from Human Brain Tissue
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Proteomics of vitamin B12 processing.

Luciana Hannibal1, Patricia M DiBello, Donald W Jacobsen

  • 1Department of Pathobiology (NC2 – 104), Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA. hannibl@ccf.org

Clinical Chemistry and Laboratory Medicine
|December 18, 2012
PubMed
Summary

Vitamin B12 (cobalamin) deficiency causes anemia and neurological issues. A study using MMACHC-mutant cells reveals significant protein alterations, suggesting irreversible damage even after hydroxocobalamin (HOCbl) treatment.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Nutritional Science

Background:

  • Cobalamin (B12, Cbl) deficiency presents multifactorial causes, including nutritional and functional impairments.
  • Major symptoms encompass megaloblastic anemia, neurological deterioration, and failure to thrive.
  • While biomarkers like hyperhomocysteinemia and methylmalonic acidemia are known, protein-level changes remain poorly understood.

Purpose of the Study:

  • To investigate the protein-level alterations in functional vitamin B12 deficiency using a cblC-disrupted (MAMC) background as a model.
  • To elucidate the mechanistic link between functional Cbl deficiency and its intracellular processing and carriers.
  • To assess the impact of hydroxocobalamin (HOCbl) supplementation on protein changes in MMACHC-mutant cells.

Main Methods:

  • Utilized a cblC-disrupted (MAMC) cellular model to study functional vitamin B12 deficiency.
  • Analyzed protein expression and pathway alterations in MMACHC-mutant cells.
  • Evaluated the efficacy of hydroxocobalamin (HOCbl) supplementation in restoring normal protein phenotypes.

Main Results:

  • Significant protein changes were observed, particularly involving the cytoskeleton, neurological system, signaling, and detoxification pathways.
  • Supplementation with hydroxocobalamin (HOCbl) did not restore MMACHC-mutant cells to a normal phenotype.
  • These findings suggest that defects in the cobalamin processing pathway can lead to irreversible protein-level damage.

Conclusions:

  • Functional vitamin B12 deficiency, modeled by MMACHC disruption, induces profound and potentially irreversible protein alterations.
  • The study highlights the complex intracellular consequences of impaired cobalamin processing beyond established biomarkers.
  • Further research is needed to understand the long-term implications and potential therapeutic strategies for irreversible protein damage in Cbl deficiency.