Results 101 to 110 of about 2,402,104 (309)
Modeling NOTCH1 driven T-cell Acute Lymphoblastic Leukemia in Mice
Bio-Protocol, 2020 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy that arises from transformation of T-cell primed hematopoietic progenitors.
Agnieszka Wendorff, Adolfo Ferrando
doaj +1 more source
A Novel t(8;14)(q24;q11) Rearranged Human Cell Line as a Model for Mechanistic and Drug Discovery Studies of NOTCH1-Independent Human T-Cell Leukemia [PDF]
, 2018 MYC-translocated T-lineage acute lymphoblastic leukemia (T-ALL) is a rare subgroup of T-ALL associated with CDKN2A/B deletions, PTEN inactivation, and absence of NOTCH1 or FBXW7 mutations.
Amadori, Alberto +12 more
core +2 more sources
Advanced Science, EarlyView.Single‐nucleus multi‐omics profiling of sinonasal squamous cell carcinoma unveils a hypoxia‐driven angiogenic axis. A specific hypoxic tumor subpopulation orchestrates endothelial tip cell differentiation via epigenetically regulated ADM and VEGFA secretion.
Chaelin You +12 more
wiley +1 more source
Genomics, 2020 Fanconi Anemia (FA) is an inherited bone marrow failure syndrome caused by mutation in FA pathway proteins, involved in Interstrand Cross Link (ICL) repair. FA cells exhibit in vitro proliferation arrest due to accumulated DNA damage, hence understanding the rescue mechanism that renders proliferation advantage is required.
Binita, Zipporah E +6 more
openaire +2 more sources
Aberrant SUMOylation Restricts the Targetable Cancer Immunopeptidome
Advanced Science, EarlyView.Pharmacological SUMOylation inhibition (SUMOi) counteracts tumor immune evasion by unmasking an immunogenic HLA‐I peptide and neoepitope repertoire. By restoring HLA‐I ligand availability through increased antigen processing and presentation, enhanced proteasomal cleavage, and modulated TAP1 peptide affinity, SUMOi boosts tumor immunogenicity ...
Uta M. Demel +19 more
wiley +1 more source
A Tie2-Notch1 signaling axis regulates regeneration of the endothelial bone marrow niche
Haematologica, 2019 Loss-of-function studies have determined that Notch signaling is essential for hematopoietic and endothelial development. By deleting a single allele of the Notch1 transcriptional activation domain we generated viable, post-natal mice exhibiting ...
Lijian Shao +12 more
doaj +1 more source
Endogenous topoisomerase II-mediated DNA breaks drive thymic cancer predisposition linked to ATM deficiency [PDF]
, 2020 The ATM kinase is a master regulator of the DNA damage response to double-strand breaks (DSBs) and a well-established tumour suppressor whose loss is the cause of the neurodegenerative and cancer-prone syndrome Ataxia-Telangiectasia (A-T).
Bernal Lozano, Cristina +10 more
core +3 more sources
Notch2 Directs aTreg Cell Fate toward Immunoregulation or Inflammatory Pyroptosis
Advanced Science, EarlyView.Schematic illustration showing that the Notch2 intracellular domain (NICD2) facilitates pyroptosis resistance in activated Tregs through the RREB1/Foxo1 signaling pathway. In addition, Notch2‐mediated pyroptosis resistance in activated Tregs promotes immunoregulatory capacity, thereby attenuating Th2‐driven inflammatory responses in allergic rhinitis ...
Yue‐Long Qiao +10 more
wiley +1 more source
NOTCH1 gain of function in germ cells causes failure of spermatogenesis in male mice.
PLoS ONE, 2013 NOTCH1 is a member of the NOTCH receptor family, a group of single-pass trans-membrane receptors. NOTCH signaling is highly conserved in evolution and mediates communication between adjacent cells.
Zaohua Huang +2 more
doaj +1 more source
Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles [PDF]
, 1996 Notch is a highly conserved transmembrane protein that is involved in cell fate decisions and is found in organisms ranging from Drosophila to humans. A human homologue of Notch, TAN1, was initially identified at the chromosomal breakpoint of a subset of
Aster, Jon C. +6 more
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