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RACK1 is up-regulated in angiogenesis and human carcinomas.

H Berns1, R Humar, B Hengerer

  • 1Cardiovascular Research Group, Department of Research, University Hospital, basel, Switzerland.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 2, 2000
PubMed
Summary

The receptor for activated C kinase 1 (RACK1) is upregulated during angiogenesis in both ovarian cycles and tumor growth. RACK1 may influence protein kinase C beta signaling in these processes.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Angiogenesis is vital for biological processes like the ovarian cycle and pathological conditions such as tumor growth.
  • Identifying key molecular players in angiogenesis is crucial for understanding and potentially treating related diseases.

Purpose of the Study:

  • To identify novel molecules involved in angiogenesis.
  • To investigate the role of the receptor for activated C kinase 1 (RACK1) in angiogenesis.

Main Methods:

  • mRNA fingerprinting and Northern blot analysis of bovine endothelial cells (EC) and corpora lutea.
  • cDNA sequencing of bovine RACK1.
  • Quantitative PCR and in situ hybridization to assess RACK1 expression in various angiogenesis models.

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Main Results:

  • RACK1 was found to be upregulated in cord-forming EC in vitro and in active corpora lutea in vivo.
  • RACK1 expression was induced during in vitro angiogenesis, murine ovarian cycle, human tumor angiogenesis, and in cancer cells.
  • RACK1 transcripts localized to proliferating EC and tumor neovascularization endothelium.

Conclusions:

  • RACK1 is significantly involved in angiogenesis across different biological contexts.
  • RACK1 expression correlates with active angiogenesis in both physiological and pathological settings.
  • RACK1 availability likely modulates protein kinase C beta (PKC beta) signaling in angiogenesis.