Concepedia

Author

Philip W. Hinds

Harvard UniversityORCID

Also Known As

Hinds, Philip W., P HINDS, P Hinds, P W Hinds, P. Hinds, P. W. Hinds, P.W. Hinds, Peter Hinds, Philip Hinds, Philip W Hinds

253

Publications

14.4K

Citations

50

H-Index

117

Concepts

All Affiliations

Harvard UniversityTufts Medical CenterMolecular Oncology (United States)Tufts UniversityPrinceton University
PW

About

Philip W. Hinds is an author at Harvard University specializing in medicine, cell biology, and tumor biology.

Top Concepts

#ConceptH-IndexPublicationsCitations

1

Medicine

36

48

11.5K

2

Health Sciences

9

9

564

3

Natural Sciences

7

7

1.8K

4

Engineering

2

2

58

5

Social Sciences

1

1

13

Philip W. Hinds

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84

Publications

13K

Citations

45

H-Index

YearCitations

The p53 proto-oncogene can act as a suppressor of transformation

Cathy A. Finlay, Philip W. Hinds, Arnold J. Levine

Cell

1989

2K

Activating mutations for transformation by p53 produce a gene product that forms an hsc70-p53 complex with an altered half-life.

Cathy A. Finlay, Philip W. Hinds, Tse‐Hua Tan,

Molecular and Cellular Biology

1988

1.1K

Regulation of retinoblastoma protein functions by ectopic expression of human cyclins

Philip W. Hinds, Sibylle Mittnacht, Vjekoslav Dulić,

Cell

1992

1K

Physical interaction of the retinoblastoma protein with human D cyclins

Steven F. Dowdy, Philip W. Hinds, Kenway Louie,

Cell

1993

761

Mutation is required to activate the p53 gene for cooperation with the ras oncogene and transformation

Philip W. Hinds, Cathy A. Finlay, Arnold J. Levine

Journal of Virology

1989

593

A common polymorphism acts as an intragenic modifier of mutant p53 behaviour

María C. Marín, Christine A. Jost, Louise Brooks,

Nature Genetics

2000

519

Function of a human cyclin gene as an oncogene.

Philip W. Hinds, Steven F. Dowdy, Elinor Ng Eaton,

Proceedings of the National Academy of Sciences

1994

459

Mutant p53 DNA clones from human colon carcinomas cooperate with ras in transforming primary rat cells: a comparison of the "hot spot" mutant phenotypes.

Philip W. Hinds, Cathy A. Finlay, Robin S. Quartin,

PubMed

1990

411

Cyclin D1 Stimulation of Estrogen Receptor Transcriptional Activity Independent of cdk4†

Elizabeth Neuman, Mohamed H. Ladha, Nancy U. Lin,

Molecular and Cellular Biology

1997

388

The Retinoblastoma Protein Acts as a Transcriptional Coactivator Required for Osteogenic Differentiation

David M. Thomas, Shannon A. Carty, Denise M. Piscopo,

Molecular Cell

2001

355

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