PRINCIPAL SCIENTIST
 Campisi, J

 SCIENTISTS
 Desprez, P
Gray, J
Huang, S
Itahana, K
Kim, S
Melov, S

 POSTDOCTORAL FELLOWS
 Davalos, A
Heo, S
Kaminker, P
Killilea, D
Krtolica, A
Lim, C
Rubio, M
You, Y

 RESEARCH ASSOCIATES
 Gao, F
Nissar, A
Zou, Y

 STUDENTS
 Kim, E
O'Day, V
Parrinello, S

 GUESTS
 Itahana, Y

 STAFF
 Staff Names Coming Soon

 


Aging is controlled by genes and the environment, and poses the largest single risk for developing a panoply of diseases, including cancer. Why do organisms age, and why do diseases such as cancer rise exponentially with age? My laboratory aims to understand the molecular and cellular basis of aging in mammals.

 

We study human and rodent cells in culture, wild-type and genetically modified mice, and -- most recently -- the simple, short-lived, genetically manipulable model organism Caenorhabditis elegans. We are exploring the causes and consequences of cellular senescence, the role of telomeres and telomere binding proteins in regulating gene expression and genomic stability, and the mechanisms by which defects in DNA repair proteins cause premature aging and cancer-prone syndromes, with an emphasis on breast cancer. We use a wide variety of techniques, ranging from molecular and cell biology to biochemistry, genetics, and computational biology.

Some specific projects that are ongoing in the lab include:
- Understanding how the p53 and pRB tumor suppressor pathways control cellular senescence.
- Using cell culture and transgenic mouse models to understand how senescent cells influence tissue function and tumorigenesis.
- Understanding the role of DNA damage, oxidative stress, and mutations in cellular senescence and organismal aging.
- Understanding how RecQ helicases, particularly those defective in Werner and Bloom syndrome, participate in DNA repair, maintain genomic stability, and suppress aging and cancer.
- Determining the regulation, function and organization of telomeres and associated proteins, and understanding how they influence cellular phenotypes and tissue function.
- Understanding how bHLH transcription factors control the growth, differentiation and apoptosis of normal and malignant mammary epithelial cells.

Judith Campisi
Senior Staff Scientist/
Life Sciences Division

One Cyclotron Rd.
Mailstop: 84-171
Berkeley, CA 94720
tel: (510)486-4416
fax: (510)486-4545
email: JCampisi@lbl.gov
 

 

 

Recent Research Publications

Itahana K, Dimri GP, Hara E, Itahana Y, Desprez P, Campisi J. (2002) A role for p53 in maintaining and establishing the quiescence growth arrest in human cells. J Biol Chem (in press).

Oshima J, Huang S, Pae C, Campisi J, Schiestl RH. (2002) Lack of WRN facilitates extensive deletion at non-homologous joining ends. Cancer Res. 62: 547-551.

Krtolica A, Parrinello S, Lockett S, Desprez P, Campisi J. (2001) Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging. Proc Natl Acad Sci USA. 98: 12072-12077.

Lim CS, Mian IS, Dernburg A, Campisi J. (2001) C. elegans clk-2, a gene that limits life span, encodes a telomere length regulator similar to yeast telomere binding protein Tel2p. Curr Biol 11: 1706-1710.

Bischof O, Kim SH, Irving J, Beresten S, Ellis NA, Campisi J. (2001) Regulation and localization of the Bloom syndrome protein in response to DNA damage. J Cell Biol 153: 367-380.

Kaminker PG, Kim SH, Taylor RD, Zebarjadian Y, Funk WD, Morin GB, Yaswen P, Campisi J. (2001) TANK2, a new TRF1-associated PARP, causes rapid induction of cell death upon overexpression. J Biol Chem 276: 35891-35899.

Bischof O, Galande S, Farzaneh F, Kohwi-Shigematsu T, Campisi J. (2001) Selective cleavage of BLM, the Bloom syndrome protein, during apoptotic cell death. J. Biol. Chem. 276: 12068-12075.

Yannone SM, Roy S, Chan D, Murphy M, Huang S, Campisi J, Chen D. (2001) Werner syndrome protein is regulated and phosphorylated by DNA-dependent protein kinase. J Biol Chem 276: 38242-38248.

Parrinello S, Lin CQ, Murata K, Itahana Y, Singh J, Krtolica A, Campisi J, Desprez PY (2001) Id-1, ITF-2 and Id-2 comprise a network of helix-loop-helix proteins that regulate mammary epithelial cell proliferation, differentiation and apoptosis. J Biol Chem 276: 39213-39219.

 

Recent Review Publications

Campisi, J. (2002) Between Scylla and Charybdis: p53 links tumor suppression and aging. Mech Ageing Dev. 123:567-573.

Kim SH, Kaminker PG, Campisi J. (2002) Telomeres, cancer and aging: In search of a happy ending. Oncogene 21: 503-511.

Campisi J, Kim, SH, Lim CS, Rubio M. (2001) Cellular senescence, cancer and aging: The telomere connection. Exp. Gerontol. 36: 1619-1637.

Campisi J. (2001) Cellular senescence as a tumor suppressor mechanism. Trends Cell Biol. 11: S27-31.