Shefali Thakur
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Shefali Thakur has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Helena Paszekova
BIOCEV, 1st Medical Faculty, Charles University, 25250 Vestec, Czech Republic
1 shared publication - Juraj Kokavec
Laboratory of Haematooncology and Stem Cells Biotechnology and Biomedicine Center of the Academy of Sciences and Charles University in Vestec (BIOCEV), First Faculty of Medicine, Charles University Prague Czech Republic
1 shared publication - Paul Kerbs
Department of Neuropathology, University Hospital Heidelberg, Heidelberg, Germany
1 shared publication - Petra Tauchmanova
BIOCEV, 1st Medical Faculty, Charles University, 25250 Vestec, Czech Republic
1 shared publication - Philipp A. Greif
German Cancer Consortium (DKTK), partner site Munich, a partnership between DKFZ and University Hospital LMU Munich Munich Germany
1 shared publication - Tereza Turkova
BIOCEV, 1st Medical Faculty, Charles University, 25250 Vestec, Czech Republic
1 shared publication
Latest Publications
- Open Access
- 18 March 2020
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 21 (6) , 2073
Loss of ISWI ATPase SMARCA5 (SNF2H) in Acute Myeloid Leukemia Cells Inhibits Proliferation and Chromatid Cohesion
ISWI chromatin remodeling ATPase SMARCA5 (SNF2H) is a well-known factor for its role in regulation of DNA access via nucleosome sliding and assembly. SMARCA5 transcriptionally inhibits the myeloid master regulator PU.1. Upregulation of SMARCA5 was previously observed in CD34+ hematopoietic progenitors of acute myeloid leukemia (AML) patients. Since high levels of SMARCA5 are necessary for intensive cell proliferation and cell cycle progression of developing hematopoietic stem and progenitor cells in mice, we reasoned that removal of SMARCA5 enzymatic activity could affect the cycling or undifferentiated state of leukemic progenitor-like clones. Indeed, we observed that CRISPR/cas9-mediated SMARCA5 knockout in AML cell lines (S5KO) inhibited the cell cycle progression. We also observed that the SMARCA5 deletion induced karyorrhexis and nuclear budding as well as increased the ploidy, indicating its role in mitotic division of AML cells. The cytogenetic analysis of S5KO cells revealed the premature chromatid separation. We conclude that deleting SMARCA5 in AML blocks leukemic proliferation and chromatid cohesion.
- 18 March 2020
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 21 (6) , 2073
Open AccessLoss of ISWI ATPase SMARCA5 (SNF2H) in Acute Myeloid Leukemia Cells Inhibits Proliferation and Chromatid Cohesion
ISWI chromatin remodeling ATPase SMARCA5 (SNF2H) is a well-known factor for its role in regulation of DNA access via nucleosome sliding and assembly. SMARCA5 transcriptionally inhibits the myeloid master regulator PU.1. Upregulation of SMARCA5 was previously observed in CD34+ hematopoietic progenitors of acute myeloid leukemia (AML) patients. Since high levels of SMARCA5 are necessary for intensive cell proliferation and cell cycle progression of developing hematopoietic stem and progenitor cells in mice, we reasoned that removal of SMARCA5 enzymatic activity could affect the cycling or undifferentiated state of leukemic progenitor-like clones. Indeed, we observed that CRISPR/cas9-mediated SMARCA5 knockout in AML cell lines (S5KO) inhibited the cell cycle progression. We also observed that the SMARCA5 deletion induced karyorrhexis and nuclear budding as well as increased the ploidy, indicating its role in mitotic division of AML cells. The cytogenetic analysis of S5KO cells revealed the premature chromatid separation. We conclude that deleting SMARCA5 in AML blocks leukemic proliferation and chromatid cohesion.