MIG-6 and SPRY2 in the Regulation of Receptor Tyrosine Kinase Signaling: Balancing Act via Negative Feedback Loops

Tumor suppressor genes (TSGs) function in concert with diverse parts of the cellular machi‐ nery and integrate the signaling networks in a cell [1]. TSGs act to safeguard the networks, to fine-tune signaling outputs, and to maintain tissue homeostasis. The loss of tumor sup‐ pressor activity or inactivation of a TSG is often due to genetic alterations such as a loss-offunction mutation or a deletion in the gene; alternatively, epigenetic silencing can result from methylation or histone modification in the TSG’s promoter regulatory elements [1-3]. Cells with a loss or a significant reduction of a particular tumor suppressor’s activity are prone to develop neoplasia in the tissues/organs where the TSG is expressed [1, 2].

• Publication year

  2013

• Venue

  Unknown venue

• Publication date

  2013-04-10

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.5772/54393
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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