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Hematopoietic stem cells lacking Ott1 display aspects associated with aging and are unable to maintain quiescence during proliferative stress.
It is shown, specifically under replicative stress, that Ott1-deleted HSCs have a significant reduction of the G(0) cell-cycle fraction associated with self-renewal and undergo early failure, establishing a requirement for Ott1 in stress hematopoiesis and suggesting thatOtt1-dependent processes may converge with those affected by aging.
PREPARATION AND EVALUATION OF TOPICAL GEL OF VALDECOXIB
Topical gels of Valdecoxib topical gel prepared using different gelling agents (Viz, carbopol, HPMC, sodium alginate, sodium CMC). Formulations were evaluated for pH, rheological behavior, drug…
Degree of Multi-tenancy and its Database for Cloud Computing
Multi-tenancy, which allows a single application to emulate multiple application instances, has been proposed as a solution to this problem. By sharing one application across many tenants,…
Ott1(Rbm15)-Deficient Hematopoietic Stem Cells Are Unable to Maintain Quiescence During Replicative Stress and Display Features of Premature Aging,
Deletion of Ott1 in adult mice utilizing Mx1-cre recapitulated certain aspects of aging hematopoiesis including increased Lin−Sca1+c-Kit+ (LSK) population, myeloid expansion and decreased lymphopoiedis, which demonstrated Ott1 is required for maintenance under competitive stress.
FLT3ITD Expression Confers the Leukemogenic Properties of Growth Factor Independence and Enhanced Self-Renewal to Yolk Sac Progenitors.
Although FLT3ITD expression in fetal liver and bone marrow allows growth factor independence, the distinctive ability to promote enhanced self-renewal as well in yolk sac cells suggests the yolksac is a uniquely vulnerable target for leukemic initiation during fetal development.