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ROR1, an embryonic protein with an emerging role in cancer biology

Protein & Cell 2014年第7期5卷 496-502页

作者： nicholas borcherding David Kusner Guang-Hui Liu Weizhou Zhang Department of Pathology College of Medicine University of Iowa Iowa City IA 52242 USA Department of Molecular and Cellular Biology College of Medicine University of Iowa Iowa City IA 52242 USA National Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China Beijing Institute for Brain Disorders Brain Tumor Center. Beiiina 100101. China

Receptor tyrosine kinase-Uke orphan receptor 1 （ROR1） is a member of the ROR family consisting of ROR1 and ROR2. RORs contain two distinct extracellular cysteinerich domains and one transmembrane domain. Within the intracellular portion, ROR1 possesses a tyrosine kinase domain, two serine/threonine-rich domains and a proline-rich domain. RORs have been studied in the context of embryonic patterning and neurogenesis through a variety of homologs. These physiologic functions are dichotomous based on the requirement of the kinase domain. A growing literature has established ROR1 as a marker for cancer, such as in CLL and other blood malignancies. In addition, ROR1 is critically involved in progression of a number of blood and solid malignancies. RORt has been shown to inhibit apoptosis, potentiate EGFR signaling, and induce epithelialmesenchymal transition （EMT）. Importantly, ROR1 is only detectable in embryonic tissue and generally absent in adult tissue, making the protein an ideal drug target for cancer therapy.

关键词： ROR1 embryogenesis cancer,immunotherapy

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Characterization of a novel mouse model with genetic deletion of CD177

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Protein & Cell 2015年第2期6卷 117-126页

作者： Qing Xie Julia Klesney-Tait Kathy Keck Corey Parlet nicholas borcherding Ryan Kolb Wei Li Lorraine Tygrett Thomas Waldschmidt Alicia Olivier Songhai Chen Guang-Hui Liu Guang-Hui Liu Xiangrui Li Weizhou Zhang College of Veterinary Medicine Nanjing Agricultural University Nanjing 210095 China Department of Pathology Holden Comprehensive Cancer Center Carver College of Medicine/University of Iowa Iowa IA 52242 USA Department of Internal Medicine Carver College of Medicine/University of Iowa Iowa IA 52242 USA Department of Pharmacology Carver College of Medicine/University of Iowa Iowa IA 52242 USA National Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China Beijing Institute for Brain Disorders Beijing 100069 China

Neutrophils play an essential role in the innate immune response to infection. Neutrophils migrate from the vasculature into the tissue in response to infection. Recently, a neutrophil cell surface receptor, CD177, was shown to help mediate neutrophil migration across the endothelium through interactions with PECAMI. We examined a publicly available gene array dataset of CD177 expression from human neutrophils following pulmonary endotoxin instillation. Among all 22,214 genes examined, CD177 mRNA was the most upregu- lated following endotoxin exposure. The high level of CD177 expression is also maintained in airspace neu- trophils, suggesting a potential involvement of CD177 in neutrophil infiltration under infectious diseases. To determine the role of CD177 in neutrophils in vivo, we constructed a CD177-genetic knockout mouse model. The mice with homozygous deletion of CD177 have no discernible phenotype and no significant change in immune cells, other than decreased neutrophil counts in peripheral blood. We examined the role of CD177 in neutrophil accumulation using a skin infection model with Staphylococcus aureus. CD177 deletion reducedneutrophil counts in inflammatory skin caused by S. aureus. Mechanistically we found that CD177 deletion in mouse neutrophils has no significant impact in CXCLI/ KC- or fMLP-induced migration, but led to significant cell death. Herein we established a novel genetic mouse model to study the role of CD177 and found that CD177 plays an important role in neutrophils.

关键词： CD177 neutrophil mouse model geneticdeletion

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