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Related Experiment Videos

CCK biosynthesis and processing: recent progress and future challenges

M C Beinfeld1

  • 1Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA 02111, USA.

Life Sciences
|January 1, 1997
PubMed
Summary
This summary is machine-generated.

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Genetic inactivation of prohormone convertase (PC1) causes a reduction in cholecystokinin (CCK) levels in the hippocampus, amygdala, pons and medulla in mouse brain that correlates with the degree of colocalization of PC1 and CCK mRNA in these structures in rat brain.

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The brain decade in debate: VIII. Peptide hormones and behavior: cholecystokinin and prolactin.

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Choresystokinin (CCK) undergoes post-translational modifications like sulfation and cleavage during biosynthesis. This review covers these processes in endocrine cells and the Cpe(fat)/Cpe(fat) mouse model.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • The regulated secretory pathway is crucial for peptide hormone production.
  • Peptide hormones undergo complex post-translational modifications for functional maturation.
  • Cholecystokinin (CCK) is a key gastrointestinal and neural peptide hormone.

Purpose of the Study:

  • To summarize the post-translational modifications of cholecystokinin (CCK) during biosynthesis.
  • To review CCK processing in endocrine cells and the Cpe(fat)/Cpe(fat) mouse model.
  • To identify remaining research challenges in CCK biosynthesis.

Main Methods:

  • Literature review of post-translational modifications in peptide biosynthesis.
  • Analysis of studies on CCK processing in endocrine cells.

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  • Examination of data from Cpe(fat)/Cpe(fat) mouse models.

    • Main Results:

    • CCK undergoes tyrosine sulfation, endoproteolytic cleavage, and carboxypeptidase trimming.
    • These modifications are essential for CCK's biological activity.
    • The Cpe(fat)/Cpe(fat) mouse model exhibits defects in carboxypeptidase E activity, impacting CCK processing.

    Conclusions:

    • Understanding CCK post-translational modifications is vital for comprehending its physiological roles.
    • Further research is needed to fully elucidate the mechanisms and regulation of CCK processing.
    • The Cpe(fat)/Cpe(fat) mouse serves as a valuable model for studying peptide processing defects.