Oxygen tension and Rac1b localization

Samantha Halpern, Celeste Nelson

Research output: Chapter in Book/Report/Conference proceedingConference contribution


The epithelial-mesenchymal transition (EMT) is a phenotypic change that enables epithelial cells to detach from one another, take on mesenchymal characteristics, and become motile. This process has been implicated in the metastasis of several types of human cancer, including breast cancer. Hypoxia, a condition under which cells are deprived of oxygen, is a common feature of breast tumors due to impaired vascular function and decreased blood flow to the tumor core. Rac1b, a splice variant of the Rac1 GTPase, is over-expressed in breast tumors and has been implicated in the promotion of EMT and the progression of breast cancer. Rac1b signaling activates NADPH oxidase, production of reactive oxygen species (ROS), and expression of EMT transcription factors such as Snail. Rac1b protein must be localized to the cell membrane in order to activate these downstream effectors and promote EMT. This study aims to identify the effects of hypoxia on Rac1b localization and downstream signaling.

Original languageEnglish (US)
Title of host publicationProceedings - 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014
PublisherInstitute of Electrical and Electronics Engineers Inc.
ISBN (Electronic)9781479937288
StatePublished - Dec 2 2014
Externally publishedYes
Event2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014 - Boston, United States
Duration: Apr 25 2014Apr 27 2014

Publication series

NameProceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC
ISSN (Print)1071-121X
ISSN (Electronic)2160-7001


Other2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014
Country/TerritoryUnited States

All Science Journal Classification (ASJC) codes

  • Bioengineering


  • EMT
  • Rac1b
  • hypoxia


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