Person
ISNI: 
0000 0001 0810 8700
https://isni.org/isni/0000000108108700
Name: 
Kaelin, W. G.
Kaelin, William G
Kaelin, William G. (Jr)
William G. Kaelin
William G. Kaelin (US-amerikanischer Onkologe)
Dates: 
born 1957-11-23
Creation class: 
article
Language material
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Creation role: 
author
Related names: 
Harvard University (isAffiliatedWith)
Titles: 
Alterations in G1/S cell-cycle control contributing to carcinogenesis.
Analysis of von Hippel-Lindau hereditary cancer syndrome: implications of oxygen sensing.
Another p53 doppelganger?
Binding of pRB to the PHD protein RBP2 promotes cellular differentiation.
Binding of the von Hippel-Lindau tumor suppressor protein to Elongin B and C.
Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor.
Bioluminescent imaging of Cdk2 inhibition in vivo
Cancer. Many vessels, faulty gene.
Cells degrade a novel inhibitor of differentiation with E1A-like properties upon exiting the cell cycle.
cellular effects of E2F overexpression., The
Chemosensitivity linked to p73 function.
Choosing anticancer drug targets in the postgenomic era.
Clusterin is a secreted marker for a hypoxia-inducible factor-independent function of the von Hippel-Lindau tumor suppressor protein.
common E2F-1 and p73 pathway mediates cell death induced by TCR activation, A
common polymorphism acts as an intragenic modifier of mutant p53 behaviour., A
concept of synthetic lethality in the context of anticancer therapy., The
CONFERENCE ON CELL CYCLE 2001
conserved region of unknown function participates in the recognition of E2F family members by the adenovirus E4 ORF 6/7 protein, A
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
Correction: p73 is a human p53-related protein that can induce apoptosis
Degradation of p53 by adenovirus E4orf6 and E1B55K proteins occurs via a novel mechanism involving a Cullin-containing complex
Degradation of the SCF component Skp2 in cell-cycle phase G1 by the anaphase-promoting complex
Deregulated transcription factor E2F-1 expression leads to S-phase entry and p53-mediated apoptosis
Detection of peptides, proteins, and drugs that selectively interact with protein targets.
Diverse Effects of Mutations in Exon II of the von Hippel-Lindau (VHL) Tumor Suppressor Gene on the Interaction of pVHL with the Cytosolic Chaperonin and pVHL-Dependent Ubiquitin Ligase Activity
Dysregulation of HIF and VEGF is a unifying feature of the familial hamartoma syndromes.
E2F-1 functions in mice to promote apoptosis and suppress proliferation
E2F-1-mediated transactivation is inhibited by complex formation with the retinoblastoma susceptibility gene product.
E2F1 as a target: promoter-driven suicide and small molecule modulators.
emerging p53 gene family, The
Expression cloning of a cDNA encoding a retinoblastoma-binding protein with E2F-like properties.
Expression pattern of the von Hippel-Lindau protein in human tissues.
Failure to prolyl hydroxylate hypoxia-inducible factor alpha phenocopies VHL inactivation in vivo.
feedback loop involving the Phd3 prolyl hydroxylase tunes the mammalian hypoxic response in vivo., A
Fluorescence-activated cell sorting of transfected cells.
FoxOs enforce a progression checkpoint to constrain mTORC1-activated renal tumorigenesis.
Functional Analysis of Novel Tumor Suppressor Proteins
Functional Analysis of the von Hippel Lindau Protein
Functions of the retinoblastoma protein.
Functions of the von Hippel-Lindau tumour suppressor protein.
Good COP1 or bad COP1? In vivo veritas.
HIF alpha targeted for VHL-mediated destruction by proline hydroxylation: Implications for O sub(2) sensing
HIF2[alpha] cooperates with RAS to promote lung tumorigenesis in mice
HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice.
How oxygen makes its presence felt
human p73 promoter: characterization and identification of functional E2F binding sites., The
Hypoxia-Inducible Factor 2 alpha N-Terminal and C-Terminal Transactivation Domains Cooperate To Promote Renal Tumorigenesis In Vivo, The
hypoxia-inducible factor 2alpha N-terminal and C-terminal transactivation domains cooperate to promote renal tumorigenesis in vivo., The
Hypoxia-Inducible Factor Linked to Differential Kidney Cancer Risk Seen with Type 2A and Type 2B VHL Mutations
Identification of a cyclin-cdk2 recognition motif present in substrates and p21-like cyclin-dependent kinase inhibitors.
Identification of cellular proteins that can interact specifically with the T/E1A-binding region of the retinoblastoma gene product.
Immunostaining of the von Hippel-Lindau gene product in normal and neoplastic human tissues.
Inhibition of HIF is necessary for tumor suppression by the von Hippel-Lindau protein
Inhibition of HIF2alpha is sufficient to suppress pVHL-defective tumor growth.
Inhibition of vascular endothelial growth factor with a sequence-specific hypoxia response element antagonist.
Innovations and challenges in renal cancer: consensus statement from the first international conference.
Innovations and challenges in renal cancer: summary statement from the Third Cambridge Conference.
Innovations and challenges in renal cell carcinoma: summary statement from the Second Cambridge Conference.
intact NEDD8 pathway is required for Cullin-dependent ubiquitylation in mammalian cells, An
Kidney cancer: now available in a new flavor.
Kinase requirements in human cells: III. Altered kinase requirements in VHL-/- cancer cells detected in a pilot synthetic lethal screen
kinesin KIF1B beta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor, The
kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor., The
Loss of hypoxia-inducible factor prolyl hydroxylase activity in cardiomyocytes phenocopies ischemic cardiomyopathy.
Loss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1
maize cDNA encoding a member of the retinoblastoma protein family: Involvement in endoreduplication, A
Many vessels, faulty gene
MDM2 suppresses p73 function without promoting p73 degradation.
Molecular basis of the VHL hereditary cancer syndrome
Molecular Biology of Kidney Cancer and Its Clinical Translation into Treatment Strategies, The
Mouse model for noninvasive imaging of HIF prolyl hydroxylase activity: Assessment of an oral agent that stimulates erythropoietin production
Mouse reporter strain for noninvasive bioluminescent imaging of cells that have undergone Cre-mediated recombination.
Mutation analysis of HIF prolyl hydroxylases (PHD/EGLN) in individuals with features of phaeochromocytoma and renal cell carcinoma susceptibility.
Myc-enhanced expression of Cul1 promotes ubiquitin-dependent proteolysis and cell cycle progression
Negative regulation of hypoxia-inducible genes by the von Hippel-Lindau protein
Negative regulation of the growth-promoting transcription factor E2F-1 by a stably bound cyclin A-dependent protein kinase
Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancer.
New cancer targets emerging from studies of the Von Hippel-Lindau tumor suppressor protein.
Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway.
p53 family update: p73 and p63 develop their own identities.
p53 gene family, The
p73 is a simian [correction of human] p53-related protein that can induce apoptosis.
Patterns of gene expression and copy-number alterations in von-hippel lindau disease-associated and sporadic clear cell carcinoma of the kidney.
Phosphorylation by casein kinase I promotes the turnover of the Mdm2 oncoprotein via the SCF(beta-TRCP) ubiquitin ligase.
Phosphorylation by Casein Kinase I Promotes the Turnover of the Mdm2 Oncoprotein via the SCFb-TRCP Ubiquitin Ligase
potent transrepression domain in the retinoblastoma protein induces a cell cycle arrest when bound to E2F sites, A
Proline hydroxylation and gene expression.
pVHL acts as an adaptor to promote the inhibitory phosphorylation of the NF-kappaB agonist Card9 by CK2.
pVHL Modification by NEDD8 Is Required for Fibronectin Matrix Assembly and Suppression of Tumor Development
pVHL19 is a biologically active product of the von Hippel-Lindau gene arising from internal translation initiation.
RBP1 Recruits Both Histone Deacetylase- Dependent and -Independent Repression Activities to Retinoblastoma Family Proteins
Rbx1, a component of the VHL tumor suppressor complex and SCF ubiquitin ligase.
Real-Time Imaging of Hypoxia based on VHL Activity
Recent insights into the functions of the retinoblastoma susceptibility gene product
Regulation of hypoxia-inducible mRNAs by the von Hippel-Lindau tumor suppressor protein requires binding to complexes containing elongins B/C and Cul2
Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex
retinoblastoma binding protein RBP2 is an H3K4 demethylase., The
Retinoblastoma protein and anaphase-promoting complex physically interact and functionally cooperate during cell-cycle exit
Retinoblastoma protein contains a C-terminal motif that targets it for phosphorylation by cyclin-cdk complexes
RETINOBLASTOMA SUSCEPTIBILITY GENE--FUNCTIONAL ANALYSIS
Role for the p53 homologue p73 in E2F-1-induced apoptosis.
SDH5 mutations and familial paraganglioma: somewhere Warburg is smiling.
Selective killing of transformed cells by cyclin/cyclin-dependent kinase 2 antagonists.
Signal Transduction by the Retinoblastoma Protein
Somatic inactivation of the PHD2 prolyl hydroxylase causes polycythemia and congestive heart failure.
Stable binding to E2F is not required for the retinoblastoma protein to activate transcription, promote differentiation, and suppress tumor cell growth.
Structure and partial genomic sequence of the human E2F1 gene.
Structure of an HIF-1alpha -pVHL complex: hydroxyproline recognition in signaling.
Structure of the VHL-ElonginC-ElonginB complex: implications for VHL tumor suppressor function.
Suppression of tumor growth through disruption of hypoxia-inducible transcription
Synthetic lethality: a framework for the development of wiser cancer therapeutics.
T/E1A-binding domain of the retinoblastoma product can interact selectively with a sequence-specific DNA-binding protein., The
Taking aim at novel molecular targets in cancer therapy.
Third International Meeting on von Hippel-Lindau disease.
transcription factor E2F-1 is a downstream target of RB action., The
Transcription of the E2F-1 gene is rendered cell cycle dependent by E2F DNA-binding sites within its promoter.
Transcriptional control by E2F
Treatment of kidney cancer: insights provided by the VHL tumor-suppressor protein.
TSC2 regulates VEGF through mTOR-dependent and-independent pathways
Tumor-selective transgene expression in vivo mediated by an E2F-responsive adenoviral vector
Tumour suppression by the human von Hippel-Lindau gene product
tyrosine kinase c-Abl regulates p73 in apoptotic response to cisplatin-induced DNA damage, The
Ubiquitination of hypoxia-inducible factor requires direct binding to the beta -domain of the von Hippel-Lindau protein
Using Synthetic Lethality to Select Cancer Drug Targets
v-Jun point mutation allows c-Jun to escape GSK3-dependent recognition and destruction by the Fbw7 ubiquitin ligase., The
VHL loss actuates a HIF-independent senescence programme mediated by Rb and p400
VHL tumour-suppressor gene paradigm, The
von Hippel-Lindau gene, kidney cancer, and oxygen sensing., The
von Hippel-Lindau gene-mediated growth suppression and induction of differentiation in renal cell carcinoma cells grown as multicellular tumor spheroids.
von Hippel-Lindau protein, HIF hydroxylation, and oxygen sensing, The
von Hippel-Lindau protein mutants linked to type 2C VHL disease preserve the ability to downregulate HIF.
Von Hippel-Lindau Tumor Suppressor Gene and Kidney Cancer, The
von Hippel-Lindau tumor suppressor gene inhibits hepatocyte growth factor/scatter factor-induced invasion and branching morphogenesis in renal carcinoma cells., The
von Hippel-Lindau Tumor Suppressor Protein and Clear Cell Renal Carcinoma, The
von Hippel-Lindau tumor suppressor protein is required for proper assembly of an extracellular fibronectin matrix, The
Von Hippel-Lindau tumor suppressor protein: new insights into oxygen sensing and cancer, The
von Hippel-Lindau tumour suppressor protein: new perspectives, The
von Hippel-Lindau tumour suppressor protein: O2 sensing and cancer., The
Contributed to or performed: 
ANNALS- NEW YORK ACADEMY OF SCIENCES
ANNUAL REVIEW OF PATHOLOG
BIOESSAYS
CANCER BIOLOGY AND THERAPY
CANCER CELL
CANCER INVESTIGATION
CLINICAL CANCER RESEARCH
GENES AND DEVELOPMENT
JOURNAL OF CLINICAL INVESTIGATION
JOURNAL- AMERICAN SOCIETY OF NEPHROLOGY
JOURNAL- NATIONAL CANCER INSTITUTE
NATURE REVIEWS CANCER
ONCOGENE -BASINGSTOKE-
Notes: 
Associated Group: Harvard University naf
Faculty, Medical
Preclinical cancer-target validation, 2018 title screen (William G. Kaelin Jr., M.D.; Harvard University)
The von Hippel-Lindau hereditary cancer syndrome, 2010 title screen (William G. Kaelin, Jr., M.D., Dana-Farber Cancer Institute and Harvard Medical School)
Sources: 
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