@article{30644cf3b9994306bf5c3b03564a4d8f,
title = "Altered receptor trafficking in Huntingtin Interacting Protein 1-transformed cells",
abstract = "The clathrin-associated protein, Huntingtin Interacting Protein 1 (HIP1), is overexpressed in multiple human epithelial tumors. Here, we report that HIP1 is a novel oncoprotein that transforms cells. HIP1-transformed cells, in contrast to RasV12-transformed cells, have dysregulation of multiple receptors involved in clathrin trafficking. Examples include upregulation of the epidermal growth factor receptor (EGFR) and the transferrin receptor. Furthermore, accumulation of transferrin and EGF in the HIP1-transformed cells was increased, and breast tumors that had EGFR expressed also had HIP1 upregulated. Thus, HIP1 overexpression promotes tumor formation and is associated with a general alteration in receptor trafficking. HIP1 is the first endocytic protein to be directly implicated in tumor formation.",
author = "Rao, {Dinesh S.} and Bradley, {Sarah V.} and Kumar, {Priti D.} and Hyun, {Teresa S.} and Djenann Saint-Dic and Katherine Oravecz-Wilson and Kleer, {Celina G.} and Ross, {Theodora S.}",
note = "Funding Information: We would like to thank Dr. Maria Soengas and Dr. Scott Lowe for the Ha-RasV12 construct; Dr. Steve Ethier and Michelle Dziubinski for the MCF10A cells and helpful advice; Pfizer, Inc. for the use of their ErbB inhibitor CI-1033; the University of Michigan Histology Core Laboratory for the IHC stains; members of the Ross laboratory, Drs. Sean Morrison, Eric Fearon, and Marisol Soengas for critical review of the manuscript; A. Ozge Yilmaz for assistance with construction of plasmids, and Kay Meisenheimer for assistance with the manuscript. This work was supported by a postdoctoral fellowship grant from the Huntington's Disease Society of America (DR), and grants from the NIH, ASH, and the Damon Runyon Foundation (TSR).",
year = "2003",
month = may,
doi = "10.1016/S1535-6108(03)00107-7",
language = "English (US)",
volume = "3",
pages = "471--482",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "5",
}