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Data indicate a pathway MYSM1/miR (zeige MLXIP Proteine)-150/FLT3 (zeige FLT3 Proteine) that inhibits proliferation of B1a cells, which may be involved in the pathogenesis of systemic lupus erythematosus (SLE).
this study shows that MYSM1 deficiency is associated with developmental aberrations, progressive bone marrow failure with myelodysplastic features, and increased susceptibility to genotoxic stress
data suggested that expression of MYSM1 was associated with the progression of CRC (zeige CALR Proteine) and might be a potential biomarker for clinical prognosis
An in vivo genetic reversion highlights the crucial role of MYSM1 in human hematopoiesis and lymphocyte differentiation
the biallelic truncation of MYSM1 likely represents the cause of an inherited bone marrow failure syndrome in two siblings
The SWIRM structure of human MYb (zeige MYB Proteine)-like, Swirm and Mpn domain-containing protein (zeige MPND Proteine)-1 (MYSM1), is reported.
The identification of histone H2A deubiquitinase (2A-DUB, or KIAA1915/MYSM1) specific for monoubiquitinated H2A (uH2A) that helps in delineating a strategy for specific regulatory pathways of gene activation, is reported.
Mysm1 enhanced function of the IRF2 and IRF8 promoters, suggesting that Mysm1 governs the IRFs for hematopoietic stem cell homeostasis.
MYSM1 activity at the prepro-B cell stage of development is important for the normal programming of B cell responses to stimulation once they complete their maturation process.
Overall we conclude that Mysm1 expression within the niche is not essential for the maintenance of hematopoietic homeostasis.
this study shows that MYSM1 is involved in the maintenance, activation and survival of CD8 (zeige CD8A Proteine)+ T cells
The results demonstrate that MYSM1 plays a critical role in Mesenchymal Stromal Cell maintenance and differentiation. This study also underscores the biological significance of deubiquitinase activity in Mesenchymal Stromal Cell function.
MYSM1 is a critical negative regulator of p53 (zeige TP53 Proteine) transcriptional programs in hematopoiesis, and its repression of Bbc3/PUMA (zeige BBC3 Proteine) expression is essential for multipotent progenitor survival, and partly contributes to maintaining hematopoietic stem cell function
this study uncovers a critical role for MYSM1 in epigenetically repressing plasma cell differentiation and antibody production, in addition to its opposing, active role in B cell development.
MYSM1 is essential for normal HSC (zeige FUT1 Proteine) function and progression of hematopoiesis in the fetal liver and HSC (zeige FUT1 Proteine) maintenance in adult bone marrow.
2 motifs in MYSM1 are essential for innate immune suppression: the SWIRM domain that interacts with TRAF3 (zeige TRAF3 Proteine) and TRAF6 (zeige TRAF6 Proteine) and the metalloproteinase domain that removed K63 polyubiquitins. MYSM1 is a key negative regulator of the innate immune system
Loss of hematopoietic stem cell function and bone marrow failure in Mysm1-knockout mice are the result of p53 (zeige TP53 Proteine) activation.
Metalloprotease that specifically deubiquitinates monoubiquitinated histone H2A, a specific tag for epigenetic transcriptional repression, thereby acting as a coactivator. Preferentially deubiquitinates monoubiquitinated H2A in hyperacetylated nucleosomes. Deubiquitination of histone H2A leads to facilitate the phosphorylation and dissociation of histone H1 from the nucleosome. Acts as a coactivator by participating in the initiation and elongation steps of androgen receptor (AR)-induced gene activation (By similarity).
histone H2A deubiquitinase MYSM1
, myb-like, SWIRM and MPN domain-containing protein 1
, Myb-like, SWIRM and MPN domain-containing protein 1