Anti-Human TNFRSF10A Recombinant Antibody (Mapatumumab) (CAT#: TAB-H48)

Meyer, Mickael, et al. "Profiling the non-genetic origins of cancer drug resistance with a single-cell functional genomics approach using predictive cell dynamics." Cell systems 11.4 (2020): 367-374. https://doi.org/10.1016/j.cels.2020.08.019

This study investigates the non-genetic origins of cancer drug resistance through a novel method called fate-seq. Fate-seq links the drug response of single cells to their transcriptomic profiles, enabling the identification of molecular factors that contribute to intrinsic drug resistance. The researchers focused on HeLa cells treated with tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL) as a proof of concept. The study demonstrated that cell dynamics could distinguish transient transcriptional states, leading to a better understanding of why some cells survive cancer treatments while others do not.
Creative Biolabs provided critical reagents that were instrumental in validating the research findings. Specifically, the therapeutic antibody mapatumumab (cat# TAB-H48) was supplied by Creative Biolabs, which played a crucial role in demonstrating the increased sensitivity of cells overexpressing SIVA1 to death receptor-mediated apoptosis. This contribution was significant as it helped confirm the potential of SIVA1 as a target gene for enhancing TRAIL-induced cell death.

Park, Jong-Sung, et al. "Targeting of dermal myofibroblasts through death receptor 5 arrests fibrosis in mouse models of scleroderma." Nature communications 10.1 (2019): 1128. https://doi.org/10.1038/s41467-019-09101-4

This research investigates how targeting death receptor 5 (DR5) can reverse fibrosis in scleroderma mouse models. The study reveals that scleroderma progression involves the conversion of resident fibroblasts into myofibroblasts (MFBs) expressing α-smooth muscle actin (α-SMA) with increased capacity to produce collagen and fibrogenic components. The researchers demonstrated that TLY012, an engineered human TNF-related apoptosis-inducing ligand (TRAIL), selectively blocks dermal fibroblast activation and induces DR-mediated apoptosis in α-SMA+ MFBs through upregulated DR5. Significantly, TLY012 reversed established skin fibrosis to near-normal skin architecture in both bleomycin-induced and tight skin-1 (Tsk-1) mouse models of scleroderma.
Creative Biolabs provided the anti-DR5 agonistic antibody (Conatumumab) and anti-DR4 agonistic antibody (Mapatumumab), which were used to validate the mechanism of DR-mediated apoptosis in myofibroblasts. These antibodies enabled the researchers to demonstrate that DR5, rather than DR4, is predominantly responsible for TLY012-induced apoptosis in activated myofibroblasts. This contribution was essential for establishing that targeting upregulated DR5 in α-SMA+ MFBs represents a viable therapeutic approach for fibrosis in scleroderma, potentially offering a new treatment strategy for this serious autoimmune condition.