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Find out how our products are being used for research.
Highlights -- a selection of the latest outstanding research using Biorbyt reagents
An international group of researchers have reported on the discovery of a Nemo-like kinase (NLK) as a potential target for DBA therapy. Through screening for new DBA targets, the group has identified a compound that inhibits NLK. Chemical and genetic inhibition of NLK increases erythroid expansion in mouse and human progenitors, including bone marrow cells from DBA patients. In DBA models and patient samples, aberrant NLK activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation. It is not observed in non-erythroid hematopoietic lineages or healthy erythroblasts. Link to article:
DBA is a congenital bone marrow failure syndrome associated with ribosomal gene mutations. DBA is characterized by anaemia, congenital anomalies, and cancer predisposition. This research, which utilised Biorbyt’s NLK (Phospho-Thr298) antibody Catalogue Number: orb157946 suggests that NLK mediates aberrant erythropoiesis in DBA and is a potential target for therapy.
South Korean scientists have recently shown that dysfunctions in the 67-kDa laminin receptor (67LR), induced by status epilepticus are involved in vasogenic edema formation, accompanied by a reduced AQP4 expression in rat piriform cortices (PC). In this study, the blockade of 67LR activated p38 MAPK and ERK1/2 signalling pathways enhanced PI3K/AKT phosphorylation in endothelial cells and astrocytes. 67LR-p38 MAPK-PI3K-AKT activation resulted in increased vascular permeability in endothelial cells; In contrast 67LR-ERK1/2-PI3K-AKT signalling regulated astroglial viability and AQP4 expression. Link to article:
This research indicates 67LR-p38 MAPK/ERK1/2-PI3K-AKT-AQP4 signalling cascades play a vital role in astroglia-vascular systems, A major therapeutic target for vasogenic edema in various neurological diseases. Biorbyt’s own ERK 1/2 antibody Catalog Number: orb160960 was used in this informative study.
An international consortium of scientists aimed to determine the role and regulatory mechanisms of ZEB2-AS1 in Acute myeloid leukaemia (AML). Their results revealed that the expression levels of ZEB2-AS1 and PLK1 were upregulated, while those of miR-122-5p were downregulated in AML tissues and cells. The knockdown of ZEB2-AS1 inhibited proliferation and induced apoptosis in vitro, and inhibited tumour growth in vivo. This research demonstrates that ZEB2-AS1 promotes cell proliferation and inhibits apoptosis, at least partly by targeting PLK1 mediated by miR-122-5p in AML cells. Link to article:
AML is an aggressive cancer that affects many people around the globe. Biorbyt is proud to say a range of our products, such as our PLK1 antibody (orb315655) and Bcl-2 antibody (orb135113) were used in this novel research.