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Communicative & Integrative Biology Volume 4, 2011 - Issue 2
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Article Addendum

How does a protein with dual mitotic spindle and extracellular matrix receptor functions affect tumor susceptibility and progression?

Patrick G. Telmer London Regional Cancer Program, London Health Sciences Center, Depts. Oncology and Biochemistry, Schulich School of Medicine, University of Western Ontario, London ON Canada Correspondence[email protected] [email protected]
,
Cornelia Tolg London Regional Cancer Program, London Health Sciences Center, Depts. Oncology and Biochemistry, Schulich School of Medicine, University of Western Ontario, London ON Canada
,
James B. McCarthy Dept. Lab. Medicine and Pathology, Tumor Biology and Research Program, Masonic Comprehensive Cancer Center/University of Minnesota, Minneapolis, MN USA
&
Eva A. Turley Dept. Lab. Medicine and Pathology, Tumor Biology and Research Program, Masonic Comprehensive Cancer Center/University of Minnesota, Minneapolis, MN USACorrespondence[email protected] [email protected]
Pages 182-185 | Received 22 Nov 2010, Accepted 22 Nov 2010, Published online: 01 Mar 2011

Figures & data

Figure 1 RHAMM/HMMR-mediated MAPK signaling and interactions. RHAMM can interact directly with ERK1, CD44 and TPX2 and RHAMM expression is co-regulated with p53 and FAK. RHAMM may act as an adapter protein targeting activated ERK to various cellular locations including the mitotic spindle and cytoskeleton. This figure was generated through the use of Ingenuity Pathways Analysis (Ingenuity® Systems, www.ingenuity.com).

Figure 1 RHAMM/HMMR-mediated MAPK signaling and interactions. RHAMM can interact directly with ERK1, CD44 and TPX2 and RHAMM expression is co-regulated with p53 and FAK. RHAMM may act as an adapter protein targeting activated ERK to various cellular locations including the mitotic spindle and cytoskeleton. This figure was generated through the use of Ingenuity Pathways Analysis (Ingenuity® Systems, www.ingenuity.com).

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