| First Author | Schaefer MA | Year | 2023 |
| Journal | Exp Hematol | Volume | 128 |
| Pages | 38-47 | PubMed ID | 37722652 |
| Mgi Jnum | J:357892 | Mgi Id | MGI:7542687 |
| Doi | 10.1016/j.exphem.2023.09.003 | Citation | Schaefer MA, et al. (2023) Physiological and regenerative functions of sterile-alpha motif protein-14 in hematopoiesis. Exp Hematol |
| abstractText | Sterile alpha-motif domain-14 (Samd14) protein expression increases the regenerative capacity of the erythroid system. Samd14 is transcriptionally upregulated and promotes cell signaling via the receptor tyrosine kinase Kit in a critical window of acute erythroid regeneration. We generated a hematopoietic-specific conditional Samd14 knockout mouse model (Samd14-CKO) to study the role of Samd14 in hematopoiesis. The Samd14-CKO mouse was viable and exhibited no steady-state hematopoietic phenotype. Samd14-CKO mice were hypersensitive to 5-fluorouracil, resulting in more severe anemia during recovery and impaired erythroid progenitor colony formation. Ex vivo, Samd14-CKO hematopoietic progenitors were defective in their ability to form mast cells. Samd14-CKO mast cells exhibited altered Kit/stem cell factor (SCF), IL-3/IL-3R signaling, and less granularity than Samd14-FL/FL cells. Our findings indicate that Samd14 promotes both erythroid and mast cell functions. The Samd14-CKO mouse phenotype exhibits striking similarities to the Kit(W/W-v) mice, which carry Kit mutations resulting in reduced tyrosine kinase-dependent signaling, causing mast cell and erythroid abnormalities. The Samd14-CKO mouse model is a new tool for studying hematologic pathologies involving Kit signaling. |
