Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis

AML1/RUNX1 is a critical transcription factor in hematopoietic cell differentiation and proliferation. From the _AML1_ gene, at least three isoforms, _AML1a_, _AML1b_ and _AML1c_, are produced through alternative splicing. AML1a interferes with the function of AML1b/1c, which are often called AML1. In the current study, we found a higher expression level of _AML1a_ in ALL patients in comparison to the controls. Additionally, AML1a represses transcription from promotor of macrophage-colony simulating factor receptor (M-CSFR) mediated by AML1b, indicating that AML1a antagonized the effect of AML1b. In order to investigate the role of _AML1a_ in hematopoiesis and leukemogenesis _in vivo_, bone marrow mononuclear cells (BMMNCs) from mice were transduced with AML1a and transplanted into lethally irradiated mice, which develop lymphoblastic leukemia after transplantation. Taken together, these results indicate that overexpression of AML1a may be an important contributing factor to leukemogenesis

Metal oxide semiconductor nanomembrane-based soft unnoticeable multifunctional electronics for wearable human-machine interfaces

Wearable human-machine interfaces (HMIs) are an important class of devices that enable human and machine interaction and teaming. Recent advances in electronics, materials, and mechanical designs have offered avenues toward wearable HMI devices. However, existing wearable HMI devices are uncomfortable to use and restrict the human body's motion, show slow response times, or are challenging to realize with multiple functions. Here, we report sol-gel-on-polymer-processed indium zinc oxide semiconductor nanomembrane-based ultrathin stretchable electronics with advantages of multifunctionality, simple manufacturing, imperceptible wearing, and robust interfacing. Multifunctional wearable HMI devices range from resistive random-access memory for data storage to field-effect transistors for interfacing and switching circuits, to various sensors for health and body motion sensing, and to microheaters for temperature delivery. The HMI devices can be not only seamlessly worn by humans but also implemented as prosthetic skin for robotics, which offer intelligent feedback, resulting in a closed-loop HMI system

16-Isopropyl-5,9-dimethyl­tetra­cyclo­[10.2.2.01,10.04,9]hexa­dec-15-ene-5,14-dimethanol

The title compound, C23H38O2, a tetra­cyclo­[10.2.2.01,10.04,9] hexa­decane structure, crystallized with four independent mol­ecules in the asymmetric unit. In the crystal, these independent mol­ecules are linked by O—H⋯O hydrogen bonds, forming a polymeric chain propagating in [100

A New Caspase-8 Isoform Caspase-8s Increased Sensitivity to Apoptosis in Jurkat Cells

Caspase-8 is a key initiator of death receptor-induced apoptosis. Here we report a novel short isoform of caspase-8 (caspase-8s), which encodes the first (Death Effector Domain) DED and part of the second DED, missing the C-terminal caspase domain. In vivo binding assays showed that transfected caspase-8s bound to (Fas-associated death domain protein) FADD, the adaptor protein in (death-induced signal complex) DISC. To investigate the potential effects of caspase-8s on cell apoptosis, Jurkat cells were stably transfected with caspase-8s. Overexpression of caspase-8s increased sensitivity to the apoptotic stimuli, Fas-agonistic antibody CH11. These results suggest that caspase-8s may act as a promoter of apoptosis through binding to FADD and is involved in the regulation of apoptosis. In addition, the results also indicate that the first DED was an important structure mediating combination between caspase-8 and FADD

AML1-ETO interacts with Sp1 and antagonizes Sp1 transactivity through RUNT domain

AbstractAML1-ETO fusion protein is observed in approximately 12% of acute myeloid leukemia. In the present research, we found that AML1-ETO is able to inhibit Sp1 transactivity. We also found that this inhibition of Sp1 transactivity by AML1-ETO is achieved by interaction between Sp1 and RUNT domain of AML1. AML1b is able to abrogate the inhibition of AML1-ETO. Since Sp1 is involved in hematopoietic cell differentiation, we proposed that AML1-ETO promotes leukemogenesis by blocking cell differentiation through inhibition of Sp1 transactivity.Structured summaryMINT-6549474: AML1-ETO (genbank_protein_gi:AAB34820) physically interacts (MI:0218) with Sp1 (uniprotkb:P08047) by anti bait coimmunoprecipitation (MI:0006)MINT-6549439: Sp1 (uniprotkb:P08047) physically interacts (MI:0218) with AML1-ETO (uniprotkb:AAB34820) by anti tag coimmunoprecipitation (MI:0007)MINT-6549458: Sp1 (uniprotkb:P08047) physically interacts (MI:0218) with AML1a (uniprotkb:Q01196-2) by anti tag coimmunoprecipitation (MI:0007