Latest Posters

Patient-derived induced pluripotent stem cells (iPSCs) enable generation of in vitro models that can recapitulate human disease phenotypes. However, conventional human iPSC differentiation protocols are often lengthy, inconsistent and difficult to scale.

To overcome these challenges, researchers have developed a proprietary gene-expression targeting strategy that can rapidly reprogram hiPSCs into pure somatic cell types in a scalable manner. This approach was used to develop a Huntington’s disease (HD) model carrying a 50CAG expansion in the huntingtin (HTT) gene.

The hypothalamic-pituitary-thyroid axis (HPT axis) is conserved across vertebrate evolution. Perturbation of thyroid hormone homeostasis (THH) can lead to adverse effects in thyroid function affecting growth, metabolism and cognitive function.

Download this poster to learn more about unbiased spatial gene expression,
application of spatial gene expression plus immunofluorescence validation and targeted analysis.

Microglia are the resident immune cells of the central nervous system and play significant roles in the regulation of homeostasis and the management of tissue response to inflammatory or pathological insults.

Basic fibroblast growth factor (bFGF) is used in neural stem cell (NSC) media to maintain multipotency. Native bFGF rapidly loses biological activity when exposed to culture conditions (37°C), Heat Stable (HS) bFGF maintains > 90% homology to the native protein and ≥ 80% biological activity, even after 72 hours of exposure to 37°C.

Download this poster to find out more about human islet amyloid polypeptide (hIAPP) and the inhibitors most successful at preventing hIAPP aggregation.

To develop a neuronal 3D spheroid culture system, we tested iPSC-derived human motor neurons and cortical glutamatergic neurons using the S-BIO PrimeSurface Ultra Low Attachment Micoplates.

BrainXell's human neuron culture platforms provide a means to model the human brain in a dish and perform in vitro functional assays. This system enables the screening of disease phenotypes and pharmacological agents that alter neuronal activity.

Spinal muscular atrophy (SMA) is an inheritable cause of infant mortality that is characterized by the loss of lower motor neurons and skeletal muscle atrophy. The degeneration of motor neurons is caused by insufficient levels of survival motor neuron (SMN) protein, which is encoded by two nearly identical genes SMN1 and SMN2. Most cases of SMA harbour homozygous deletions of the SMN1 gene and retain at least one copy of SMN2.