John A. Hickman focuses on Apoptosis, Programmed cell death, Cell biology, Cancer research and Cell. John A. Hickman interconnects Molecular biology, Small intestine and Stem cell in the investigation of issues within Apoptosis. His studies in Programmed cell death integrate themes in fields like Cytotoxic T cell, DNA damage and Drug resistance.
His work in Cell biology tackles topics such as Autophagy which are related to areas like Gene knockdown and Protein structure. John A. Hickman has researched Cancer research in several fields, including Gene expression profiling, Radioresistance, Cytotoxicity, Tumor suppressor gene and Clonogenic assay. His work deals with themes such as Mammary gland involution, Immunology, Drug and Basement membrane, which intersect with Cell.
His primary areas of study are Apoptosis, Cell biology, Programmed cell death, Molecular biology and Stereochemistry. His Apoptosis research is multidisciplinary, relying on both Cell, Cancer research, Cell culture, Small intestine and Immunology. His work in Cell biology covers topics such as Bcl-2-associated X protein which are related to areas like Etoposide.
His Programmed cell death study combines topics in areas such as DNA damage, Mechanism of action, Toxicity, Cytotoxic T cell and Clonogenic assay. His study explores the link between Molecular biology and topics such as In vivo that cross with problems in Pharmacology. His research integrates issues of Biochemistry, Aryl, Alkoxy group, Alkyl and Chemical synthesis in his study of Stereochemistry.
John A. Hickman mainly focuses on Alkyl, Group, Medicinal chemistry, Stereochemistry and Aryl. His Medicinal chemistry research incorporates themes from Nitrogen atom and Hydrogen. His Stereochemistry research incorporates elements of Imide and Chemical synthesis.
His Aryl research includes themes of Ring, Alkoxy group and Tricyclic. The concepts of his Toxicity study are interwoven with issues in Cell culture, Apoptosis and In vivo. In his work, John A. Hickman performs multidisciplinary research in Apoptosis and RNA interference.
The scientist’s investigation covers issues in Cell biology, Pharmacology, Cancer cell, Cancer and Bcl-xL. His work blends Cell biology and Biphenyl compound studies together. His Biphenyl compound study spans across into areas like Programmed cell death, Plasma protein binding, BCL-2 Gene Family, Apoptosis and Puma.
His Pharmacology study combines topics in areas such as Bevacizumab, Myeloid Cell Leukemia Sequence 1 Protein and Receptor tyrosine kinase. His Cancer cell research is multidisciplinary, incorporating elements of Bcl-2 Homologous Antagonist-Killer Protein, Tumor progression, Leukemia, MCL1 and Drug discovery. His studies in Cancer integrate themes in fields like Ex vivo, Stromal cell, Stem cell and Kinase.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Apoptotic death in epithelial cells: cleavage of DNA to 300 and/or 50 kb fragments prior to or in the absence of internucleosomal fragmentation.
F. Oberhammer;J.W. Wilson;C. Dive;I.D. Morris.
The EMBO Journal (1993)
Functional and physical interaction between Bcl‐XL and a BH3‐like domain in Beclin‐1
M Chiara Maiuri;Gaëtane Le Toumelin;Alfredo Criollo;Alfredo Criollo;Alfredo Criollo;Jean-Christophe Rain.
The EMBO Journal (2007)
Apoptosis induced by anticancer drugs.
John A. Hickman.
Cancer and Metastasis Reviews (1992)
The role of p53 in spontaneous and radiation-induced apoptosis in the gastrointestinal tract of normal and p53-deficient mice.
Anita J. Merritt;Christopher S. Potten;Christopher J. Kemp;John A. Hickman.
Cancer Research (1994)
The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models
András Kotschy;Zoltán Szlavik;James Murray;James Davidson.
Cell Damage-induced Conformational Changes of the Pro-Apoptotic Protein Bak In Vivo Precede the Onset of Apoptosis
Gareth J. Griffiths;Laurence Dubrez;Clive P. Morgan;Neil A. Jones.
Journal of Cell Biology (1999)
Drug-target interactions: only the first step in the commitment to a programmed cell death?
C. Dive;J. A. Hickman.
British Journal of Cancer (1991)
BH3-only proteins and BH3 mimetics induce autophagy by competitively disrupting the interaction between Beclin 1 and Bcl-2/Bcl-X(L).
Maria Chiara Maiuri;Alfredo Criollo;Ezgi Tasdemir;Jose Miguel Vicencio.
Antitumor Activity and Pharmacokinetics in Mice of 8-Carbamoyl-3-methyl-imidazo[5,1-d]-1,2,3,5-tetrazin-4(3H)-one (CCRG 81045; M & B 39831), a Novel Drug with Potential as an Alternative to Dacarbazine
Malcolm F. G. Stevens;John A. Hickman;Simon P. Langdon;David Chubb.
Cancer Research (1987)
Differential expression of bcl-2 in intestinal epithelia. Correlation with attenuation of apoptosis in colonic crypts and the incidence of colonic neoplasia.
Anita J Merritt;Christopher S Potten;A J Watson;D Y Loh.
Journal of Cell Science (1995)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: