Ruhee Dere
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View article: 43AURKA connects NSD1 and SETD2 in an epigenetic axis governing mitotic fidelity in ccRCC
43AURKA connects NSD1 and SETD2 in an epigenetic axis governing mitotic fidelity in ccRCC Open
Background Chromothripsis-driven 3p deletion and 5q amplification are early, clonal events in clear cell renal cell carcinoma (ccRCC). These lesions respectively target the epigenetic regulators SETD2 and NSD1. Paradoxically, although NSD1…
View article: 16 Linking VHL and SETD2 in a common oncogenic pathway that converges on the mitoticspindle
16 Linking VHL and SETD2 in a common oncogenic pathway that converges on the mitoticspindle Open
Background Loss of chromosome 3p is a landmark event in clear cell renal cell carcinoma (ccRCC) that results in mono-allelic loss of VHL (von Hippel Lindau) and SETD2 (Set-domain containing 2) (and other tumor suppressors co-located on 3p)…
View article: Lysine Demethylase 4A is a Centrosome Associated Protein Required for Centrosome Integrity and Genomic Stability
Lysine Demethylase 4A is a Centrosome Associated Protein Required for Centrosome Integrity and Genomic Stability Open
Centrosomes play a fundamental role in nucleating and organizing microtubules in the cell and are vital for faithful chromosome segregation and maintenance of genomic stability. Loss of structural or functional integrity of centrosomes cau…
View article: Figure S4 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S4 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
CENP/B and CREST status of micronuclei
View article: Figure S3 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S3 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Multiple Setd2w/f MEF clones display reduced aTubK40me3 protein (A) and relative Setd2 mRNA (B) levels
View article: Figure S5 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S5 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Reduced SETD2 levels promote genomic instability without compromising H3K36 trimethylation.
View article: Figure S2 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S2 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
SETD2 loss promotes chromosomal abnormalities.
View article: Supplementary Fig Legends from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Supplementary Fig Legends from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
fig legends for sup figures
View article: Data from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Data from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Loss of the short arm of chromosome 3 (3p) occurs early in >95% of clear cell renal cell carcinoma (ccRCC). Nearly ubiquitous 3p loss in ccRCC suggests haploinsufficiency for 3p tumor suppressors as early drivers of tumorigenesis. We previ…
View article: Data from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Data from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Loss of the short arm of chromosome 3 (3p) occurs early in >95% of clear cell renal cell carcinoma (ccRCC). Nearly ubiquitous 3p loss in ccRCC suggests haploinsufficiency for 3p tumor suppressors as early drivers of tumorigenesis. We previ…
View article: Figure S4 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S4 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
CENP/B and CREST status of micronuclei
View article: Supplementary Fig Legends from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Supplementary Fig Legends from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
fig legends for sup figures
View article: Figure S6 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S6 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Human tumor analysis
View article: Figure S3 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S3 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Multiple Setd2w/f MEF clones display reduced aTubK40me3 protein (A) and relative Setd2 mRNA (B) levels
View article: Figure S5 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S5 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Reduced SETD2 levels promote genomic instability without compromising H3K36 trimethylation.
View article: Figure S6 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S6 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Human tumor analysis
View article: Figure S1 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S1 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Micronuclei are a Common Feature among ccRCC-derived Cell Lines.
View article: Figure S1 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S1 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
Micronuclei are a Common Feature among ccRCC-derived Cell Lines.
View article: Figure S2 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma
Figure S2 from <i>SETD2</i> Haploinsufficiency for Microtubule Methylation Is an Early Driver of Genomic Instability in Renal Cell Carcinoma Open
SETD2 loss promotes chromosomal abnormalities.
View article: Data from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
Data from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27 Open
Tuberin, the Tsc2 gene product, integrates the phosphatidylinositol 3-kinase/mitogen-activated protein kinase (mitogenic) and LKB1/AMP-activated protein kinase (AMPK; energy) signaling pathways, and previous independent studies have…
View article: Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27 Open
Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
View article: Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27 Open
Supplementary Figures 1-2, Table 1 from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
View article: Data from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27
Data from AMP-Activated Protein Kinase Signaling Results in Cytoplasmic Sequestration of p27 Open
Tuberin, the Tsc2 gene product, integrates the phosphatidylinositol 3-kinase/mitogen-activated protein kinase (mitogenic) and LKB1/AMP-activated protein kinase (AMPK; energy) signaling pathways, and previous independent studies have…
View article: SETD2 safeguards the genome against isochromosome formation
SETD2 safeguards the genome against isochromosome formation Open
Summary Factors governing the faithful replication of chromosomes are essential for cellular and genomic integrity. While a variety of mechanisms to manage breaks and promote repair of DNA are widely recognized, epigenetic landmarks that p…
View article: Author Correction: Therapeutically actionable signaling node to rescue AURKA driven loss of primary cilia in VHL-deficient cells
Author Correction: Therapeutically actionable signaling node to rescue AURKA driven loss of primary cilia in VHL-deficient cells Open
View article: Mechanistic insights into KDM4A driven genomic instability
Mechanistic insights into KDM4A driven genomic instability Open
Alterations in global epigenetic signatures on chromatin are well established to contribute to tumor initiation and progression. Chromatin methylation status modulates several key cellular processes that maintain the integrity of the genom…
View article: A Cytoskeletal Function for PBRM1 Reading Methylated Microtubules
A Cytoskeletal Function for PBRM1 Reading Methylated Microtubules Open
The chromatin modifier SETD2 was recently shown to be a dual-function methyltransferase that “writes” methyl marks on both chromatin and the mitotic spindle, revealing α-tubulin methylation as a new posttranslational modification of microt…
View article: SETD2 is an actin lysine methyltransferase
SETD2 is an actin lysine methyltransferase Open
SET-domain-containing-2 (SETD2) was identified as the methyltransferase responsible for the histone 3 lysine 36 trimethyl (H3K36me3) mark of the histone code. Most recently, SETD2 has been shown to be a dual-function remodeler that regulat…
View article: Ubiquitination and regulation of AURKA identifies a hypoxia-independent E3 ligase activity of VHL
Ubiquitination and regulation of AURKA identifies a hypoxia-independent E3 ligase activity of VHL Open
View article: Methylated α-tubulin antibodies recognize a new microtubule modification on mitotic microtubules
Methylated α-tubulin antibodies recognize a new microtubule modification on mitotic microtubules Open
Posttranslational modifications (PTMs) on microtubules differentiate these cytoskeletal elements for a variety of cellular functions. We recently identified SETD2 as a dual-function histone and microtubule methyltransferase, and methylatio…