Section: Publications

Postdoctoral Position Available

Michelle Kelliher, Ph.D.

Academic Role: Associate Professor

Faculty Appointment(s) In:
   Cancer Biology
   Molecular Genetics and Microbiology

Other Affiliation(s):
   Center for AIDS Research
   Interdisciplinary Graduate Program
   Program in Immunology and Virology

Recent Publications:

Kelliher MA, Seldin DC, Leder P (1996). Tal-1 induces T cell acute lymphoblastic leukemia accelerated by casein kinase IIa. EMBO J., 5 (19): 5160-5166.

Kelliher MA, Grimm S, Ishida Y, Kuo F, Leder P. (1998). The death domain kinase RIP mediates the TNF-a induced NF-kB signal. Immunity, 8: 297-303.

Devin A, Cook A, Lin Y, Rodriguez Y, Kelliher M, Liu Z. (2000). The distinct roles of TRAF2 and RIP in TNFR1-mediated IKK activation: IKK is recruited into the TNFR1 complex via TRAF2 while its activation is mediated by RIP. Immunity 12, 419-429.

Lin Y, Devin A, Cook A, Keane M, Kelliher M, Lipkowitz S, Liu Z. (2000). The death domain kinase RIP is essential for TRAIL (Apo2L)-induced activation of IkB kinase and c-jun N-terminal kinase. Mol. and Cell. Biol. 20: 6638-6645.

O’Neil J, Billa M, Oikemus S, Kelliher MA. (2001). The DNA binding activity of TAL-1 is not required to induce leukemia/lymphoma in mice. Oncogene 20, 3897-3905.

Cusson N, Oikemus S, Kilpatrick ED, Cunningham L, Kelliher M. (2002). The death domain kinase RIP protects thymocytes from tumor necrosis factor receptor type 2-induced cell death.  J Exp Med. 196:15-26.

O'Neil J, Ventura JJ, Cusson N, Kelliher M.  (2003).  NF-kappaB activation in premalignant mouse tal1/scl thymocytes and tumors.  Blood 102(7):2593-6.

Lee TH, Huang Q, Oikemus S, Shank J, Ventura JJ, Cusson N, Vaillancourt RR, Su B, Davis RJ, Kelliher MA. (2003).  The death domain kinase RIP1 is essential for tumor necrosis factor alpha signaling to p38 mitogen-activated protein kinase.  Mol Cell Biol. 23:8377-85. 

Meylan E, Burns K, Hofmann K, Blancheteau V, Martinon F, Kelliher M., Tschopp J. (2004).  RIP1 is an essential mediator of Toll-like receptor 3-induced NF-kappa B activation.  Nat Immunol.5(5):503-7.

O'Neil J, Shank J, Cusson N, Murre C, Kelliher M. (2004). Tal1/scl induces leukemia by inhibiting the transcriptional activity of E47/HEB.  Cancer Cell (in press).

Lee TH, Shank J, Cusson N, Kelliher M.  (2004).  The kinase activity of Rip1 is not required for TNF-a-induced Ikk or p38 MAP kinase activation or for the ubiquitination of Rip1 by Traf 2.  J.Biol.Chem. (in press).

Vivarelli M, McDonald D, Miller M, Cusson N, Kelliher M, Geha RS. (2004).  Rip 1 links TLR4 to Akt and is essential for cell survival in response to LPS stimulation.  J. Exp Med.  200:399-404.

Das S, Cho J, Lambertz I, Kelliher MA, Eliopoulos AG, Du K, Tsichlis P. (2005).  Tpl2/Cot signals activate ERK, JNK and NF-kB in a cell-type and stimulus-specific manner.  J. Biol. Chem 280:23748-23757.

Cusson-Hermance N, Khurana S, Lee TH, Fitzgerald KA, Kelliher MA. (2005).  Rip1 mediates the Trif-dependent Toll-like receptor 3 and 4-induced NF-kB activation but does not contribute to IRF-3 activation.  J. Biol. Chem.  280: 36560-6.

O,Neil J, Calvo J, McKenna K, Krishnamoorthy V, Aster JC, Bassing CH, Alt FW, *Kelliher M,  *Look AT.  (2006).  Activating Notch1 mutations in mouse models of T-ALL.  Blood 107:781-5.  (*senior co-authors).

Shank-Calvo J, Draheim K, Bhasin M,  Kelliher MA.  (2006).  p16Ink4a or p19Arf loss contributes to Tal1-induced leukemogenesis in mice. Oncogene, 25:3023-31.

Chang PY, Draheim K, Kelliher MA, Miyamoto S.  (2006).  NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells.  Cancer Research, 66:6008-13.

Sharma VM*, Calvo JA*, Draheim K, Cunningham L, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco A, Kelliher MA.  (2006).  Notch1 contributes to mouse T cell leukemia by directly inducing the expression of c-myc.  Mol. Cell. Biol. [E ahead of print 5 Sept. 2006] (* equal contribution).

Office: LRB-421
Phone: 508-856-8620
E-mail: Michelle.Kelliher@umassmed.edu
Keywords: Genetic Systems, Cancer Biology, Signal Transduction

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Postdoctoral Position Available A postdoctoral position is available to study in this laboratory. Contact Dr. Kelliher for additional details.