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Physiological functions and signaling partners of Nore1

Nore1 (Nore1A and Nore1B) was identified as a potential Ras effector because it can bind Ras in a GTP dependent fashion and the binding requires an intact Ras effector domain. Recent studies have shown that Nore1 is a negative regulator of cell proliferation and is one of the two genes that are disrupted due to chromosomal translocation in a familial clear cell renal cell carcinoma. Nore1A expression is extremely low in a variety of cancer cell lines. Nore1 promoter hypermethylation has been reported in some cancer tissues and cancer cell lines. Nore1 is also homologous to Rassf1A, a recently identified bona fide tumor suppressor whose expression is lost in many types of cancer cells due to promoter hypermethylation. Nore1 and Rassf1 can form heterodimers in vivo.

My research interest is focused on identifying the signaling partners and elucidating the molecular mechanisms involved in negative regulation of cell proliferation by Nore1. I am also interested in exploring the potential role of Nore1 in cellular differentiation related to mammalian neural, immune and skin systems.

References

1. Vavvas D, Li X, Avruch J, Zhang XF, Identification of Nore1 as a potential new Ras effector, J Biol. Chem. 1998;273;5439-5442

2. Ortiz-Vega S, Khokhlatchev A, Nedwidek M, Zhang XF, Damman G, Pfeifer G, Avruch J, The putative tumor supressor Rassf1 homodimerizes and heterodimerizes with the Ras-GTP binding protein Nore1, Oncogene, 2002;21;1381-1390

3. Khokhlatchev A, Xavier R, Rabizadeh S, Nedwidek M, Chen T, Zhang XF, Seed B, Avruch J, Identification of a novel Ras-regulated proapoptotic pathway, Current Biology, 2002;12;253-265

4. Tommasi S, Dammann R, Jin SG, Zhang XF, Avruch J, Pfeifer G, RASSF3 and NORE1: identification and cloning of two human homologues of the putative tumor suppressor gene RASSF1, Oncogene, 2002;21;2713-2720

5. Aoyama Y, Avruch J, Zhang XF, NORE1 inhibits tumor cell growth independent of Ras or the MST1/2 kinases, Oncogene, 2004;23:3426-3433.


	Xian-feng Zhang, Ph.D. Physiological functions and signaling partners of Nore1 Nore1 (Nore1A and Nore1B) was identified as a potential Ras effector because it can bind Ras in a GTP dependent fashion and the binding requires an intact Ras effector domain. Recent studies have shown that Nore1 is a negative regulator of cell proliferation and is one of the two genes that are disrupted due to chromosomal translocation in a familial clear cell renal cell carcinoma. Nore1A expression is extremely low in a variety of cancer cell lines. Nore1 promoter hypermethylation has been reported in some cancer tissues and cancer cell lines. Nore1 is also homologous to Rassf1A, a recently identified bona fide tumor suppressor whose expression is lost in many types of cancer cells due to promoter hypermethylation. Nore1 and Rassf1 can form heterodimers in vivo. My research interest is focused on identifying the signaling partners and elucidating the molecular mechanisms involved in negative regulation of cell proliferation by Nore1. I am also interested in exploring the potential role of Nore1 in cellular differentiation related to mammalian neural, immune and skin systems. References 1. Vavvas D, Li X, Avruch J, Zhang XF, Identification of Nore1 as a potential new Ras effector, J Biol. Chem. 1998;273;5439-5442 2. Ortiz-Vega S, Khokhlatchev A, Nedwidek M, Zhang XF, Damman G, Pfeifer G, Avruch J, The putative tumor supressor Rassf1 homodimerizes and heterodimerizes with the Ras-GTP binding protein Nore1, Oncogene, 2002;21;1381-1390 3. Khokhlatchev A, Xavier R, Rabizadeh S, Nedwidek M, Chen T, Zhang XF, Seed B, Avruch J, Identification of a novel Ras-regulated proapoptotic pathway, Current Biology, 2002;12;253-265 4. Tommasi S, Dammann R, Jin SG, Zhang XF, Avruch J, Pfeifer G, RASSF3 and NORE1: identification and cloning of two human homologues of the putative tumor suppressor gene RASSF1, Oncogene, 2002;21;2713-2720 5. Aoyama Y, Avruch J, Zhang XF, NORE1 inhibits tumor cell growth independent of Ras or the MST1/2 kinases, Oncogene, 2004;23:3426-3433.