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Pradip Raychaudhuri

Researcher at Howard Hughes Medical Institute

Publications -  10
Citations -  1011

Pradip Raychaudhuri is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Transcription factor & E2F. The author has an hindex of 9, co-authored 10 publications receiving 1004 citations. Previous affiliations of Pradip Raychaudhuri include Research Triangle Park.

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Journal ArticleDOI

Adenovirus E1A proteins can dissociate heteromeric complexes involving the E2F transcription factor: A novel mechanism for E1A trans-activation

TL;DR: A function for E1A is demonstrated in mediating a dissociation of transcription factor complexes, allowing new interactions to form and thus changing the transcriptional specificity.
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Domains of the adenovirus E1A protein required for oncogenic activity are also required for dissociation of E2F transcription factor complexes.

TL;DR: Isolation of a cellular activity can reconstitute the E2F-cyclin-A complex and has permitted a more detailed analysis of the mechanism of E1A dissociation, which finds that sequences in conserved region 1 (CR1) and Conserved region 2 (CR2) are important for dissociation of the E 2F complex, whereas amino-terminal sequences are not required.
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Identification of an E1A-inducible cellular factor that interacts with regulatory sequences within the adenovirus E4 promoter.

TL;DR: An analysis of proteins which bind to the E4 promoter in an attempt to define the basis for E1A control of this gene finds that one of these factors, termed E4F, is increased at least 10‐fold in extracts prepared from Ad5 infected cells and that the increase requires the E 1A gene.
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Analysis of trans activation by human papillomavirus type 16 E7 and adenovirus 12S E1A suggests a common mechanism.

TL;DR: E7 trans activation is functionally related to that mediated by the 12S E1A product, and biochemical studies demonstrate that the E7 protein can alter the interaction of cellular factors with the E2F transcription factor.
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DNA-binding activity of the adenovirus-induced E4F transcription factor is regulated by phosphorylation.

TL;DR: The activation process appears to involve a phosphorylation event, because treatment of E4F with alkaline phosphatase abolishes activity and incubation of theosphatase-inactivated factor with an extract from virus infected cells restores activity.