Ask about this productRelated genes to: SAMD14 antibody
- Gene:
- SAMD14 NIH gene
- Name:
- sterile alpha motif domain containing 14
- Previous symbol:
- -
- Synonyms:
- FLJ36890
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-13
- Date modifiied:
- 2014-11-19
Related products to: SAMD14 antibody
Related articles to: SAMD14 antibody
- Samd14 coordinates stem cell factor/Kit receptor signaling and is crucial for the survival of erythroid precursors in anemia contexts. Here, we show that Samd14 is needed to maintain balanced autophagy in erythroid precursors following acute anemia. Autophagy-associated gene signatures and protein levels are deregulated when erythropoiesis accelerates in acute anemia. Mechanistically, Samd14 interacts via its SAM domain with phosphatidylinositol 3-phosphate (PI3P), an integral component of endosomal and autophagic membranes. Pharmacologic inhibition of VPS34, the class III PI 3-kinase that generates PI3P, impaired erythroid differentiation specifically in stress contexts. Loss of Samd14 shifted the sensitivity of erythroid precursors to VPS34 inhibition, where higher doses were required to block differentiation. Given the critical roles of autophagy in normal differentiation, Samd14's stress-dependent activation and roles in autophagy suggest that this mechanism is needed to maintain progenitor levels and balance the production of healthy, mature red blood cells in anemia. - Source: PubMed
Publication date: 2026/03/02
Roy PoojaRose Blake ARay SuhitaDogiparthi Venkatasai RSchaefer Meg AStucky Cheryl LChoi SuyongWoods Nicholas THewitt Kyle J - Samd14 is crucial for cell signaling and survival in mouse models of acute anemia. Samd14 has an N-terminal actin capping protein (CP) and a C-terminal sterile alpha motif (SAM) to coordinate stem cell factor/Kit and erythropoietin receptor signaling pathways during terminal differentiation of red blood cell precursors. Here we present new findings that Samd14 expression is needed to maintain balanced autophagy in red blood cell precursors following acute anemia. Autophagy gene signatures and protein levels are markedly altered within the context of acute anemia when red blood cell precursors accelerate the process of erythropoiesis. Samd14 interacted via its SAM domain with phosphatidylinositol 3-phosphate (PI3P) which is an integral component of endosomal and autophagic membranes. We tested PI3Ps role in red blood cell differentiation using a small molecule inhibitor of the Class III PI 3-kinase VPS34, which is the sole kinase responsible for PI3P genesis. SAR405 treatment blocked red blood cell formation. In the absence of Samd14, higher doses of VPS34 inhibition were required to block erythroid differentiation. Given the critical roles of autophagy in normal differentiation, Samd14's stress-dependent activation and roles in autophagy suggest that this mechanism is needed to maintain progenitor levels and balance the production of healthy, mature red blood cells. - Source: PubMed
Publication date: 2025/08/19
Roy PoojaRose Blake ARay SuhitaSchaefer Meg ADogiparthi Ventakasai RChoi SuyongWoods Nicholas THewitt Kyle J - This review evaluates the known mechanisms of regulating erythroid regeneration via the sterile alpha motif protein-14 ( Samd14 ) enhancer, Samd14's role in stem cell factor/Kit and erythropoietin (Epo) signaling, possible SAMD14 functions beyond erythropoiesis, and extrapolation to other anemia-response pathways. - Source: PubMed
Publication date: 2025/04/24
Hewitt Kyle JRoy PoojaSchaefer Meg A - Primary vitreoretinal lymphoma (PVRL) is a rare subtype of DLBCL and can progress into primary central nervous system lymphoma (PCNSL). To investigate the role of chronic antigenic stimulation in PVRL, we cloned and expressed B-cell receptors (BCR) from PVRL patients and tested for binding against human auto-antigens. SEL1L3, a protein with multiple glycosylation sites, was identified as the BCR target in 3/20 PVRL cases. SEL1L3 induces proliferation and BCR pathway activation in aggressive lymphoma cell lines. Moreover, SEL1L3 conjugated to a toxin killed exclusively lymphoma cells with respective BCR-reactivity. Western Blot analysis indicates the occurrence of hyper-N-glycosylation of SEL1L3 at aa 527 in PVRL patients with SEL1L3-reactive BCRs. The BCR of a PVRL patient with serum antibodies against SEL1L3 was cloned from a vitreous body biopsy at diagnosis and of a systemic manifestation at relapse. VH4-04*07 was used in both lymphoma manifestations with highly conserved CDR3 regions. Both BCRs showed binding to SEL1L3, suggesting continued dependence of lymphoma cells on antigen stimulation. These results indicate an important role of antigenic stimulation by post-translationally modified auto-antigens in the genesis of PVRL. They also provide the basis for a new treatment approach targeting unique lymphoma BCRs with ultimate specificity. - Source: PubMed
Publication date: 2024/04/26
Elbert MichelleNeumann FrankKiefer MaximilianChristofyllakis KonstantinosBalensiefer BenediktKos IgorCarbon GabiKaddu-Mulindwa DominicBittenbring Joerg ThomasFadle NatalieRegitz EviFend FalkoBonzheim IrinaThurner LorenzBewarder Moritz - The development and progression of hepatocellular carcinoma (HCC) have been reported to be associated with immune-related genes and the tumor microenvironment. Nevertheless, there are not enough prognostic biomarkers and models available for clinical use. Based on seven prognostic genes, this study calculated overall survival in patients with HCC using a prognostic survival model and revealed the immune status of the tumor microenvironment (TME). - Source: PubMed
Li Meng-TingZheng Kai-FengQiu Yi-Er