StemSpan™ SFEM
Serum-free medium for culture and expansion of hematopoietic cells
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Overview
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (12)
Publications (340)
Septin7 is essential in early hematopoiesis, but redundant at later stages.
Life science alliance 2026 Oct
Abstract
The unique cytoskeletal protein Septin7 is generally considered to be required for cytokinesis in yeast and mammals. Whole-body genetic ablation of Septin7 in mice is embryonically lethal. Septin7-deficient fibroblasts and HeLa cells are defective in cytokinesis and undergo obligate multinucleation. Surprisingly, lymphocyte- and myeloid-specific deletion of Septin7 in mice caused no detectable defects in blood lineage development, indicating dispensability of Septin7 for hematopoiesis. However, Septin7-deficient hematopoietic stem cells failed to engraft and establish donor chimerism after transplantation. To reconcile these contradictory findings, we examined the consequences of Septin7 deletion at distinct stages of hematopoiesis. Our results demonstrate that Cre-induced deletion of the floxed Septin7 allele is inefficient during the early stages of hematopoiesis, suggesting strong selection pressure against Septin7 deficiency at this stage. In contrast, deletion of Septin7 at the common lymphoid progenitor stage, as well as in Hoxb8-immortalized hematopoietic progenitors, is efficient and does not result in any noticeable defects in cell division. Taken together, our findings indicate that Septin7 is essential during early hematopoiesis but becomes dispensable at later stages.
Temporal Lysophosphatidic Acid Supplementation Enhances Megakaryocyte Differentiation and Platelet Production From Human Hematopoietic Progenitors.
Cell biology international 2026 Jun
Abstract
Platelet shortages and limited storage stability restrict global platelet transfusion capacity, highlighting the need for efficient in vitro platelet production systems. This study establishes a simple, non-genetic and cost-effective system for efficient in vitro platelet-like particle (PLP) production from human hematopoietic stem/progenitor cells (HSPCs) using a Phase-specific modulation of Hippo-YAP/TAZ signaling modulation. Temporal control of Hippo-YAP/TAZ signaling by lysophosphatidic acid (LPA), an activator of YAP/TAZ activity, significantly enhanced megakaryocyte differentiation, expansion and PLP production, resulting in an approximately 15-fold increase in PLP yield at the end of the procedure. Furthermore, LPA extended the expansion period of HSPC-derived megakaryocytes up to 8 days, resulting in a greater than 20-fold increase in the number of HSPC-derived CD41+ megakaryocytes. Moreover, replacement of expensive commercial recombinant human thrombopoietin (C-rhTPO), one of the major cost-driving components in in vitro PLP production, with recombinant human thrombopoietin produced in Escherichia coli (W-rhTPO) further improved the cost-effectiveness of the procedure. In conclusion, this study demonstrates that temporally controlled Hippo-YAP/TAZ signaling, together with affordable cytokine supplementation, provides a robust and GMP-compatible platform for large-scale PLP manufacturing for future clinical applications. We believe that this system will enable scalable PLP generation, even in resource-constrained settings, to increase human platelet supply for many life-saving therapies in the future.
DLK1 is a GATA1s-driven dependency and therapeutic target in Down syndrome-associated myeloid leukemia.
Blood advances 2026 Jun
Abstract
Children with Down syndrome have a markedly increased risk of developing myeloid leukemia. Although having an excellent prognosis, 10% to 20% develop relapsed or refractory disease with poor survival, highlighting the need for new targeted approaches. The pathogenesis of myeloid leukemia of Down syndrome (ML-DS) is tightly linked to fetal hematopoiesis and mutations in GATA1, generating the truncated GATA1 short (GATA1s) isoform. We identified Delta-like noncanonical Notch ligand 1 (DLK1) as a direct GATA1s target. DLK1, a paternally imprinted transmembrane protein, is highly expressed in fetal liver CD34+ cells but absent in adult hematopoiesis, making it an attractive immunotherapeutic target. Chromatin profiling revealed GATA1s occupancy at a distal enhancer within the DLK1-DIO3 locus, driving aberrant DLK1 upregulation in ML-DS. Functional studies demonstrated that DLK1 is a leukemia dependency, as its genetic ablation impaired proliferation and engraftment, induced apoptosis, and altered Notch and β-catenin signaling. Therapeutically, a DLK1-directed antibody-drug conjugate-induced selective cytotoxicity, abrogated colony formation, and significantly prolonged survival in refractory ML-DS patient-derived xenograft (PDX) models, achieving durable remissions at higher doses. These findings establish DLK1 as a leukemia-specific vulnerability and provide preclinical proof-of-concept for DLK1-targeted therapies in ML-DS and other leukemias with fetal-like expression programs.
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Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
