Yasuyuki Sera
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View article: JMJD3-mediated senescence is required to overcome stress-inducedhematopoietic defects
JMJD3-mediated senescence is required to overcome stress-inducedhematopoietic defects Open
Cellular senescence in stem cells compromises regenerative capacity, promotes chronic inflammation, and is implicated in aging. Hematopoietic stem and progenitor cells (HSPCs) are responsible for producing mature blood cells, however, how …
View article: JMJD3 mediated senescence is required to overcome stress induced hematopoietic defects
JMJD3 mediated senescence is required to overcome stress induced hematopoietic defects Open
Cellular senescence in stem cells compromises regenerative capacity, promotes chronic inflammation, and is implicated in aging. Hematopoietic stem and progenitor cells (HSPCs) are responsible for producing mature blood cells, however, how …
View article: PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1
PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1 Open
The genome is constantly exposed to DNA damage from endogenous and exogenous sources. Fine modulation of DNA repair, chromatin remodeling, and transcription factors is necessary for protecting genome integrity, but the precise mechanisms a…
View article: PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1
PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1 Open
The genome is constantly exposed to DNA damage from endogenous and exogenous sources. Fine modulation of DNA repair, chromatin remodeling, and transcription factors is necessary for protecting genome integrity, but the precise mechanisms a…
View article: MBTD1 preserves adult hematopoietic stem cell pool size and function
MBTD1 preserves adult hematopoietic stem cell pool size and function Open
Mbtd1 (mbt domain containing 1 ) encodes a nuclear protein containing a zinc finger domain and four malignant brain tumor (MBT) repeats. We previously generated Mbtd1 -deficient mice and found that MBTD1 is highly expressed in fetal hemato…
View article: Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction
Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction Open
Purpose:Epigenetic deregulation is deeply implicated in the pathogenesis of bladder cancer. KDM6A (Lysine (K)-specific demethylase 6A) is a histone modifier frequently mutated in bladder cancer. However, the molecular mechanisms of how KDM…
View article: Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction
Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction Open
Purpose:Epigenetic deregulation is deeply implicated in the pathogenesis of bladder cancer. KDM6A (Lysine (K)-specific demethylase 6A) is a histone modifier frequently mutated in bladder cancer. However, the molecular mechanisms of how KDM…
View article: Supplementary Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction
Supplementary Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction Open
Supplementary Information: Tables S1, S2, S3, S4 (gene set enrichment analyses); Figures S1, S2, S3, S4
View article: Supplementary Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction
Supplementary Data from <i>Kdm6a</i> Deficiency Activates Inflammatory Pathways, Promotes M2 Macrophage Polarization, and Causes Bladder Cancer in Cooperation with <i>p53</i> Dysfunction Open
Supplementary Information: Tables S1, S2, S3, S4 (gene set enrichment analyses); Figures S1, S2, S3, S4
View article: Exploration of Oncogenic Functions Targeting the DNA Methylation Factors UTX/UTY in Renal Cell Carcinoma
Exploration of Oncogenic Functions Targeting the DNA Methylation Factors UTX/UTY in Renal Cell Carcinoma Open
DNA methylation and histone modifications are crucial for tissue homeostasis, and mutations in methylation-related genes like UTX and UTY are closely associated with cancer development. In renal cell carcinoma (RCC), defects in UTX and UTY…
View article: UTX maintains the functional integrity of the murine hematopoietic system by globally regulating aging-associated genes
UTX maintains the functional integrity of the murine hematopoietic system by globally regulating aging-associated genes Open
Epigenetic regulation is essential for the maintenance of the hematopoietic system, and its deregulation is implicated in hematopoietic disorders. In this study, UTX, a demethylase for lysine 27 on histone H3 (H3K27) and a component of COM…
View article: Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation
Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation Open
Additional sex combs like 1 (ASXL1) is frequently mutated in myeloid malignancies and clonal hematopoiesis of indeterminate potential (CHIP). Although loss of ASXL1 promotes hematopoietic transformation, there is growing evidence that ASXL…
View article: Acquired expression of CblQ367P in mice induces dysplastic myelopoiesis mimicking chronic myelomonocytic leukemia
Acquired expression of CblQ367P in mice induces dysplastic myelopoiesis mimicking chronic myelomonocytic leukemia Open
Key Points Acquired expression of CblQ367P induces sustained proliferation of myelomonocytes, multilineage dysplasia, and splenomegaly resembling CMML. Combined inhibition of PI3K and JAK2 efficiently suppressed the growth of CblQ367P-indu…
View article: Propagation of trimethylated H3K27 regulated by polycomb protein EED is required for embryogenesis, hematopoietic maintenance, and tumor suppression
Propagation of trimethylated H3K27 regulated by polycomb protein EED is required for embryogenesis, hematopoietic maintenance, and tumor suppression Open
Significance Polycomb repressive complex 2 (PRC2) is a central regulator in all forms of histone H3 Lys27 (H3K27) methylation. Interaction of embryonic ectoderm development (EED) with trimethylated H3K27 (H3K27me3) is required for the allo…
View article: Maintenance of the functional integrity of mouse hematopoiesis by EED and promotion of leukemogenesis by EED haploinsufficiency
Maintenance of the functional integrity of mouse hematopoiesis by EED and promotion of leukemogenesis by EED haploinsufficiency Open
View article: Identification of cooperative genes for <i>E2A‐PBX1</i> to develop acute lymphoblastic leukemia
Identification of cooperative genes for <i>E2A‐PBX1</i> to develop acute lymphoblastic leukemia Open
E2A‐ PBX 1 is a chimeric gene product detected in t(1;19)‐bearing acute lymphoblastic leukemia ( ALL ) with B‐cell lineage. To investigate the leukemogenic process, we generated conditional knock‐in ( cKI ) mice for E2A‐ PBX 1 , in which E…