Редактирование: TP53INP1

Tumor protein p53-inducible nuclear protein 1 (Stress-induced protein) (p53-dependent damage-inducible nuclear protein 1) (p53DINP1) [P53DINP1] [SIP]

==Publications==

{{medline-entry
|title=[[TP53INP1]] deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30559202
|abstract=Bone marrow (BM) produces all blood and immune cells deriving from hematopoietic stem cells (HSCs). The decrease of immune cell production during aging is one of the features of immunosenescence. The impact of redox dysregulation in BM aging is still poorly understood. Here we use [[TP53INP1]]-deficient (KO) mice endowed with chronic oxidative stress to assess the influence of aging-associated redox alterations in BM homeostasis. We show that [[TP53INP1]] deletion has no impact on aging-related accumulation of HSCs. In contrast, the aging-related contraction of the lymphoid compartment is mitigated in [[TP53INP1]] KO mice. B cells that accumulate in old KO BM are differentiating cells that can mature into functional B cells. Importantly, this phenotype results from B cell-intrinsic events associated with defective redox control. Finally, we show that oxidative stress in aged [[TP53INP1]]-deficient mice maintains STAT5 expression and activation in early B cells, driving high [i]Pax5[/i] expression, which provides a molecular mechanism for maintenance of B cell development upon aging.
|mesh-terms=* Aging
* Animals
* B-Lymphocytes
* Bone Marrow
* Lymphopoiesis
* Male
* Mice
* Mice, Inbred C57BL
* Nuclear Proteins
* Oxidation-Reduction
* Oxidative Stress
* Receptors, Interleukin-7
* STAT5 Transcription Factor
* Signal Transduction
|keywords=* aging
* early B cell differentiation
* hematopoiesis
* immunosenescence
* oxidative stress
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320535
}}