p202 is a protein expressed in murine cells after Interferon treatment. Although the function of p202 is still basically unknown, its ability to bind the hypophosphorylated form of the retinoblastoma protein pRb suggests a possible role in the control of cell proliferation. To investigate the role of p202 we have generated several cell clones of NIH 3T3 fibroblasts that constitutively express p202. Here we show that proliferation of quiescent cells on stimulation by serum addition is strongly inhibited by constitutive p202 expression. Moreover, when growth arrested cells are stimulated to proliferate, expression of p202 inhibits G0/G1 progression into the S phase and the cells accumulate with a DNA content that is equivalent to cells arrested in the G0/G1 phase of the cell cycle. Taken together, these studies suggest that p202 may play a negative role in growth regulation.

Constitutive expression of the interferon-inducible protein p202 in NIH 3T3 cells affects cell cycle progression.

LEMBO, David;NOVELLI, Francesco;LANDOLFO, Santo Giuseppe
1995

Abstract

p202 is a protein expressed in murine cells after Interferon treatment. Although the function of p202 is still basically unknown, its ability to bind the hypophosphorylated form of the retinoblastoma protein pRb suggests a possible role in the control of cell proliferation. To investigate the role of p202 we have generated several cell clones of NIH 3T3 fibroblasts that constitutively express p202. Here we show that proliferation of quiescent cells on stimulation by serum addition is strongly inhibited by constitutive p202 expression. Moreover, when growth arrested cells are stimulated to proliferate, expression of p202 inhibits G0/G1 progression into the S phase and the cells accumulate with a DNA content that is equivalent to cells arrested in the G0/G1 phase of the cell cycle. Taken together, these studies suggest that p202 may play a negative role in growth regulation.
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LEMBO D ;ANGERETTI A ;BENEFAZIO S ;HERTEL L ;GARIGLIO M ;NOVELLI F ;LANDOLFO S
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/31025
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