Asrij/OCIAD1 suppresses CSN5-mediated p53 degradation and maintains mouse hematopoietic stem cell quiescence

Inactivation of the tumor suppressor p53 is essential for unrestrained growth of cancers. However, only 11% of hematological malignancies have mutant p53. Mechanisms that cause wild-type p53 dysfunction and promote leukemia are inadequately deciphered. The stem cell protein Asrij/OCIAD1 is misexpres...

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Veröffentlicht in:	Blood 2019-05, Vol.133 (22), p.2385-2400
Hauptverfasser:	Sinha, Saloni, Dwivedi, Tirath Raj, Yengkhom, Roja, Bheemsetty, Venkata Anudeep, Abe, Takaya, Kiyonari, Hiroshi, VijayRaghavan, K., Inamdar, Maneesha S.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Differentiation Cell Division COP9 Signalosome Complex - genetics COP9 Signalosome Complex - metabolism Disease Models, Animal F-Box Proteins - genetics F-Box Proteins - metabolism Hematopoiesis Hematopoietic Stem Cells Mice Mice, Knockout Myeloproliferative Disorders - genetics Myeloproliferative Disorders - metabolism Myeloproliferative Disorders - pathology Peptide Hydrolases - genetics Peptide Hydrolases - metabolism Proteolysis Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism
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