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Related Concept Videos

Translation01:31

Translation

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Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Proteins are...
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Translation01:31

Translation

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Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
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Mutations01:39

Mutations

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Overview
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Mutations01:35

Mutations

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Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
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Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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Related Experiment Video

Updated: Mar 12, 2026

Laser Capture Microdissection of Mouse Embryonic Cartilage and Bone for Gene Expression Analysis
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Laser Capture Microdissection of Mouse Embryonic Cartilage and Bone for Gene Expression Analysis

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TRIC-B Mutations Causing Osteogenesis Imperfecta.

Atsuhiko Ichimura1, Hiroshi Takeshima

  • 1Graduate School of Pharmaceutical Sciences, Kyoto University.

Biological & Pharmaceutical Bulletin
|November 3, 2016
PubMed
Summary

Trimeric intracellular cation channel B (TRIC-B) mutations cause osteogenesis imperfecta by impairing bone ossification. Tric-b-knockout mice reveal the disease mechanism, highlighting TRIC-B

Area of Science:

  • Cellular Biology
  • Molecular Medicine
  • Genetics

Background:

  • Trimeric intracellular cation (TRIC) channels, TRIC-A and TRIC-B, are located in intracellular membranes and facilitate monovalent cation transport.
  • TRIC channels are implicated in calcium (Ca2+) release from intracellular stores.
  • Genetic mutations in TRIC-B have been linked to autosomal recessive osteogenesis imperfecta (OI).

Purpose of the Study:

  • To investigate the molecular mechanism underlying TRIC-B mutations in osteogenesis imperfecta.
  • To establish and utilize a Tric-b knockout mouse model for studying OI.
  • To elucidate the role of TRIC-B in bone ossification.

Main Methods:

  • Generation and analysis of Tric-b knockout mice.
  • Histological and cellular studies on Tric-b knockout bones.

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  • Investigation of cultured cell lines derived from OI patients with TRIC-B mutations.

    • Main Results:

    • Tric-b knockout mice exhibit impaired bone ossification, serving as a relevant OI model.
    • Studies revealed key aspects of the pathophysiology in TRIC-B-mutated OI.
    • TRIC-B channels play an essential role in the process of bone ossification.

    Conclusions:

    • TRIC-B is crucial for proper bone ossification.
    • Understanding TRIC-B channel function is vital for addressing osteogenesis imperfecta.
    • TRIC-B mutations present a significant molecular mechanism for OI pathogenesis.