YAP and TAZ (WWTR1) are transcriptional co-activators that play a central role in the Hippo Signaling pathway that regulates cell, tissue and organ growth. Under growth conditions, YAP and TAZ are translocated to the nucleus, where they interact with DNA-binding transcription factors (e.g., Transcriptional Enhanced Activation Domain [TEAD] proteins) to regulate the expression of genes that control fundamental aspects of cell function, such as proliferation and cell survival (1). A number of genes have been experimentally confirmed as targets of transcriptional regulation by YAP and TAZ. These include the extracellular matrix proteins CTGF, CYR61, and integrin β2 (2-4), the inhibitor of apoptosis protein (IAP) survivin (5), the mechano-sensitive nuclear envelope protein Lamin B2 (6), and the oncogenic receptor tyrosine kinase Axl (7).

Literature Sharing: Microglia-specific Regulation of Lipid Metabolism in Alzheimer's Disease I. Research Background Alzheimer's disease (AD), as the most common neurodegenerative disease and major cause of dementia, is characterized by severe disruption of brain homeostasis as one of its core pathological features. The role of abnormal lipid metabolism in disease progression has long been insufficiently recognized. In recent years, with the development of lipidomics technology, studies have found that imbalances in lipids such as phospholipids, sphingolipids, and cholesterol may be initiating factors in AD pathogenesis, rather than mere pathological byproducts. These lipid disorders can promote amyloidogenesis through mechanisms such as regulating membrane fluidity, secretase compartmentalization, and Aβ aggregation kinetics. The study "Microglia-specific regulation of lipid metabolism in Alzheimer's disease revealed by microglial depletion in 5xFAD Mice" focuses on microglia—the brain's resident immune cells. Combining the 5xFAD transgenic mouse model with human post-mortem brain tissue samples, the study investigates the specific regulatory role of microglia in lipid metabolism disorders in AD. The aim is to decipher the association between abnormal lipid metabolism in AD and different brain cell types and molecular pathways, providing new therapeutic targets for the disease. Previous studies have confirmed that lipid metabolism risk genes enriched in microglia (such as TREM2, PLCG2, GRN, etc.) are involved in Aβ clearance and neuroinflammation regulation. However, the specific impact of microglial depletion on brain lipid metabolism has been widely overlooked, with only one study focusing on its necessity for leukotriene synthesis, which became the core entry point for this study.

β-catenin is a key downstream effector in the Wnt signaling pathway (1). It is implicated in two major biological processes in vertebrates: early embryonic development (2) and tumorigenesis (3). CK1 phosphorylates β-catenin at Ser45. This phosphorylation event primes β-catenin for subsequent phosphorylation by GSK-3β (4-6). GSK-3β destabilizes β-catenin by phosphorylating it at Ser33, Ser37, and Thr41 (7). Mutations at these sites result in the stabilization of β-catenin protein levels and have been found in many tumor cell lines (8).

Synapses are the site for brain communication where information is transmitted between neurons and stored for memory formation.

It is now considered that OPCs as neuroectoderm-origin multipotent progenitors that are NG2/PDGFRα positive, highly ramified, mainly generating OLs, but are also capable of giving rise to other CNS cell types including astrocytes.

Neurons are the cells that give rise to our perceptions, memories, and behaviors. They do so by communicating through dense, intricate networks of synapses, the neuron-to-neuron junctions through which neurons transmit chemical (neurotransmitter) and electrical signals.

Neuroectodermal markers are a class of biomolecules that are specifically expressed in cells derived from the embryonic neuroectoderm, including proteins, enzymes, receptors, and transcription factors. They are primarily expressed in neurons, glial cells, neuroendocrine cells, neural crest cells, and their corresponding tumor cells.

Neurodegenerative diseases are characterised by selective dysfunction and loss of synaptic connectivity and neurons.

There is no "universal loading control", only the most suitable loading control for your experimental conditions. The key is to make a reasonable selection based on your cell line/tissue source, treatment conditions, and the molecular weight of the target protein.

The γ secretase protease complex interacts with and cleaves intramembrane substrates as an essential function for regulation of intracellular signaling and cell-cell interactions. This multiprotein complex is comprised of four integral membrane proteins, Presenilin, Nicastrin, Aph-1, and PEN2, all of which are essential for complete proteolytic activity (1). Presenilin 1 and presenilin 2 are transmembrane proteins belonging to the presenilin family.