A5043387899- Pancreatic and Hepatic Oncology Research
- Cancer-related Molecular Pathways
- Cancer, Lipids, and Metabolism
- Lung Cancer Treatments and Mutations
- Endoplasmic Reticulum Stress and Disease
- Ubiquitin and proteasome pathways
- Cancer, Hypoxia, and Metabolism
- RNA modifications and cancer
- Phagocytosis and Immune Regulation
- Hepatocellular Carcinoma Treatment and Prognosis
- Metabolomics and Mass Spectrometry Studies
- Cell death mechanisms and regulation
- FOXO transcription factor regulation
- Neuroblastoma Research and Treatments
- Microtubule and mitosis dynamics
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- Virus-based gene therapy research
- Genomics and Chromatin Dynamics
- Cancer Mechanisms and Therapy
- Protein Degradation and Inhibitors
- Signaling Pathways in Disease
- Glycosylation and Glycoproteins Research
- Pancreatic function and diabetes
- Cancer Genomics and Diagnostics
University of Cambridge
2014-2023
Chinese Academy of Medical Sciences & Peking Union Medical College
2018
Addenbrooke's Hospital
1997-2014
Cornell University
2011
Papworth Hospital
2008
Ludwig Cancer Research
1985-2007
MRC Laboratory of Molecular Biology
1985-2002
Medical Research Council
2002
The Honourable Society of Lincoln's Inn
1990-2000
St Bartholomew's Hospital
1990
Journal Article A modified oestrogen receptor ligand-binding domain as an improved switch for the regulation of heterologous proteins Get access Trevor D. Littlewood, Littlewood * Biochemistry Cell NucleusLondon WC2A 3PX, UK To whom correspondence should be addressed Search other works by this author on: Oxford Academic PubMed Google Scholar David C. Hancock, Hancock Paul S. Danielian, Danielian 1Molecular Endocrinology Laboratories, Imperial Cancer Research Fund, PO Box 123, 44 Lincoln's...
The two oncogenes KRas and Myc cooperate to drive tumorigenesis, but the mechanism underlying this remains unclear. In a mouse lung model of
Vascular smooth muscle cell (VSMC) accumulation is implicated in plaque development. In contrast, VSMC apoptosis rupture, coagulation, vessel remodeling, medial atrophy, aneurysm formation, and calcification. Although accompanies multiple pathologies, there little proof of direct causality, particularly with the low levels seen vivo. Using a mouse model inducible VSMC-specific apoptosis, we demonstrate that low-level during either atherogenesis or within established plaques apolipoprotein...
Abstract The signature features of pancreatic ductal adenocarcinoma (PDAC) are its fibroinflammatory stroma, poor immune activity, and dismal prognosis. We show that acute activation Myc in indolent intraepithelial neoplasm (PanIN) epithelial cells vivo is, alone, sufficient to trigger immediate release instructive signals together coordinate changes multiple stromal immune-cell types drive transition adenocarcinomas share all the characteristic their spontaneous human counterpart. also...
Philippe Juin, Anne-Odile Hueber, Trevor Littlewood, and Gerard Evan Imperial Cancer Research Fund, London WC2A 3PX, UK
The site-directed recombinase Cre can be employed to delete or express genes in cell lines animals. Clearly, the ability control remotely activity of this enzyme would highly desirable. To end we have constructed expression vectors for fusion proteins consisting and a mutated hormone-binding domain murine oestrogen receptor. latter still binds anti-oestrogen drug tamoxifen but no longer 17β-oestradiol. We show here that embryonic stem cells expressing such proteins, efficiently induce...
The interaction between nuclear pore proteins (nucleoporins) and transport factors is crucial for the translocation of macromolecules through pores. Many nucleoporins contain FG sequence repeats, previous studies have demonstrated interactions repeats containing FxFG or GLFG cores factors. crystal structure residues 1-442 importin-beta bound to a peptide indicates that this repeat core binds same primary site as cores. Importin-beta-I178D shows reduced binding both consistent with an...
DNA damage and the response have been identified in human atherosclerosis, including vascular smooth muscle cells (VSMCs). However, although double-stranded breaks (DSBs) are hypothesized to promote plaque progression instability, part, by promoting cell senescence, apoptosis, inflammation, direct effects of DSBs VSMCs seen atherogenesis unknown.To determine presence effect endogenous levels on atherosclerosis.Human atherosclerotic showed increased expression multiple proteins vitro vivo,...
c-Myc promotes apoptosis by destabilizing mitochondrial integrity, leading to the release of proapoptotic effectors including holocytochrome c. Candidate mediators in this process are members Bcl-2 family. We show here that fibroblasts lacking Bak remain susceptible c-Myc-induced whereas bax-deficient resistant. However, despite requirement for Bax, activation exerts no detectable effects on Bax expression, localization, or conformation. Moreover, susceptibility can be restored cells ectopic...
Abstract The recent demonstration that apoptosis of vascular smooth muscle cells (VSMCs) occurs in human atherosclerotic plaques suggests VSMC may promote plaque rupture and subsequent myocardial infarction. In culture, VSMCs show higher rates than from normal vessels, although the mechanism this effect is unknown. earlier studies, we have shown tumor suppressor gene p53 regulates rat after deregulated cell cycle control. We therefore analyzed function cultured derived coronary or media...