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Automated and standardized colony counting for the hematopoietic colony-forming unit (CFU) assay
Now Available: ³§°Õ·¡²Ñ±¹¾±²õ¾±´Ç²Ôâ„¢ 21 CFR Part 11 Compliance Software Add-On (Catalog #500-0110). Request pricing above for more information.
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³§³¾²¹°ù³Ù¶Ù¾±²õ³óâ„¢Meniscus-free cultureware for more accurate counting of hematopoietic colonies in CFU assays
What Our Product Engineer Says
We developed ³§°Õ·¡²Ñ±¹¾±²õ¾±´Ç²Ôâ„¢ as our own "expert CFU counter in a box" and to remove some of the subjectivity inherent in counting colonies in a CFU assay. Using standardized algorithms helps to reduce variations that might be seen when different people are counting and scoring colonies manually.
Oliver EgelerSenior Systems Engineer
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Resources and Publications
Educational Materials (22)
Publications (21)
FSL-1 Pre-Administration Protects Radiation-Induced Hematopoietic Organs Through the Modulation of the TLR Signaling Pathway
International Journal of Molecular Sciences 2025 May
Abstract
Substantial progress has been made in the development of radiation countermeasures, resulting in the recent approval of several mitigators; however, there has yet to be an approved prophylactic radioprotectant. Research on countermeasure performance in mixed neutron and gamma radiation fields has also been scarce. Fibroblast-stimulating lipopeptide (FSL-1) is a novel synthetic agonist for toll-like receptor 2/6. In previous studies, the administration of FSL-1 before and after gamma radiation significantly improved survival outcomes for mice through the activation of the NF-κB pathway. In the current study, we tested FSL-1’s radioprotective abilities in a mixed radiation field that models one produced by a nuclear detonation in 11–14-week-old C57BL/6 male and female mice. We demonstrate that a single dose of 1.5 mg/kg of FSL-1 administered 12 h prior to 65% neutron 35% gamma mixed-field (MF) irradiation enhances survival, accelerates recovery of hematopoietic cell and stem cell populations, reduces inflammation, and protects innate immune function in mice. FSL-1’s ability to recover blood and protect immune functions is important in countering the high rate of incidence of sepsis caused by MF radiation’s damaging effects. These results demonstrate that FSL-1 is a promising prophylactic countermeasure where exposure to MF radiation is anticipated.
Characterization of E1 enzyme dependencies in mutant- UBA1 human cells reveals UBA6 as a novel therapeutic target in VEXAS syndrome
Leukemia 2025 Jun
Abstract
VEXAS syndrome is a clonal hematopoietic disorder characterized by hyperinflammation, bone marrow failure, and high mortality. The molecular hallmark of VEXAS is somatic mutations at methionine 41 (M41) in the E1 ubiquitin enzyme, UBA1. These mutations induce a protein isoform switch, but the mechanisms underlying disease pathogenesis remain unclear. Here, we developed a human cell model of VEXAS syndrome by engineering the male monocytic THP1 cell line to express the common UBA1 M41V mutation. We found that mutant UBA1 M41V cells exhibit aberrant UBA1 isoform expression, increased vacuolization, and upregulation of the unfolded protein response, recapitulating key features of VEXAS. Moreover, proteomic analyses revealed dysregulated ubiquitination and proteotoxic stress in UBA1 M41V cells, with alterations in inflammatory and stress-response pathways. Functional studies demonstrated that UBA1 M41V cells were highly sensitive to genetic or pharmacological inhibition of E1 ubiquitin enzymes. Treatment with the E1 enzyme inhibitor TAK-243 preferentially suppressed colony formation of UBA1 M41V cells as compared to WT cells. Moreover, UBA1 M41V cells exhibited greater sensitivity to TAK-243 in competition assays and showed increased apoptosis. Interestingly, TAK-243 preferentially inhibited UBA6 activity over UBA1, suggesting that UBA6 may compensate for UBA1 dysfunction in UBA1 M41V cells. Targeting UBA6 using shRNA or the UBA6-specific inhibitor phytic acid further revealed an acquired dependency on UBA6 in UBA1 M41V cells. Phytic acid selectively impaired growth and colony formation in UBA1 M41V cells while sparing WT cells, highlighting a potential therapeutic vulnerability. Together, these findings establish a novel human model of VEXAS syndrome, identify key roles for UBA1 and UBA6 in disease pathogenesis, and demonstrate that UBA6 inhibition represents a promising therapeutic strategy for selectively targeting UBA1 mutant clones. Subject terms: Haematological cancer, Cell signalling
High frequency CCR5 editing in human hematopoietic stem progenitor cells protects xenograft mice from HIV infection
Nature Communications 2025 Jan
Abstract
The only cure of HIV has been achieved in a small number of people who received a hematopoietic stem cell transplant (HSCT) comprising allogeneic cells carrying a rare, naturally occurring, homozygous deletion in the CCR5 gene. The rarity of the mutation and the significant morbidity and mortality of such allogeneic transplants precludes widespread adoption of this HIV cure. Here, we show the application of CRISPR/Cas9 to achieve >90% CCR5 editing in human, mobilized hematopoietic stem progenitor cells (HSPC), resulting in a transplant that undergoes normal hematopoiesis, produces CCR5 null T cells, and renders xenograft mice refractory to HIV infection. Titration studies transplanting decreasing frequencies of CCR5 edited HSPCs demonstrate that <90% CCR5 editing confers decreasing protective benefit that becomes negligible between 54% and 26%. Our study demonstrates the feasibility of using CRISPR/Cas9/RNP to produce an HSPC transplant with high frequency CCR5 editing that is refractory to HIV replication. These results raise the potential of using CRISPR/Cas9 to produce a curative autologous HSCT and bring us closer to the development of a cure for HIV infection. Subject terms: HIV infections, CRISPR-Cas9 genome editing, Retrovirus, Translational research
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Now Available: ³§°Õ·¡²Ñ±¹¾±²õ¾±´Ç²Ôâ„¢ 21 CFR Part 11 Compliance Software Add-On (Catalog #500-0110). Request pricing above for more information.
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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 º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
