生命科学科研大百科

Cannabinoid receptors mediate a number of physiological processes in the brain ranging from appetite regulation, pain, learning, and memory. The major cannabinoid receptors in the brain include CB1 and CB2 receptors, which are G-protein coupled receptors (GPCRs). CB1 interacts with other GPCRs including metabotropic glutamate receptor 1, mGluR1. Endogenous ligands, endocannabinoids, but also exogenously introduced compounds such as tetrahydrocannabinol (THC), activate cannabinoid receptors by promoting the exchange of GDP for GTP, leading to a cascade of signaling pathways that are activated to drive various functions.

Cancer-associated Growth Factor The tumor microenvironment (TME) is composed of a heterogenous mixture of tumor cells, blood vessels, fibroblasts, stromal cells, infiltrating immune cells, and extracellular matrix (ECM) components, whose collective interactions play important roles in tumor development [1]. Cells in the TME secrete a variety of bioactive molecules, including growth factors, cytokines, ECM proteins, and proteases (e.g., MMPs), many of which play critical roles in regulating growth and development of the tumor[2,3].

This article focuses on calcium transport-related proteins and their regulatory mechanisms, with an emphasis on the SERCA family of proteins, the regulatory protein PLN, and the PKA kinase activated by the second messenger cAMP. These three components collectively participate in the fine regulation of intracellular calcium concentration.

The tumor microenvironment (TME) has been shown to play an important role in tumor initiation, development, and metastasis. Numerous factors contribute to the nature of the TME such as the presence of immune cells; T-cells, B-cells, and natural killer (NK) cells, and wider environmental factors, such as extracellular matrix (ECM) stiffness, hypoxia, and interstitial pressure. Amongst all these various factors, fibroblasts have been suggested to play a key role in tumor development.

Cadherin-Catenin The tumor microenvironment (TME) has been shown to play an important role in tumor initiation, development, and metastasis. Numerous factors contribute to the nature of the TME such as the presence of immune cells; T-cells, B-cells, and natural killer (NK) cells, and wider environmental factors, such as extracellular matrix (ECM) stiffness, hypoxia, and interstitial pressure. Amongst all these various factors, fibroblasts have been suggested to play a key role in tumor development.

The modulation of chromatin structure is an essential component in the regulation of transcriptional activation and repression. Modifications can be made by at least two evolutionarily conserved strategies, through the disruption of histone-DNA contacts by ATP-dependent chromatin remodelers, or by histone tail modifications including methylation and acetylation.

ER stress-induced autophagy is the core mechanism by which cells respond to protein homeostasis imbalances.

Chaperone-mediated autophagy (CMA) is a process triggering the lysosomal-mediated degradation of specific protein targets. CMA is induced by a variety of stresses, including starvation, genotoxic insults, oxidative stress, and hypoxia.

ATM (Ataxia Telangiectasia Mutated) is a serine/threonine protein kinase best known for its role in the DNA damage signaling cascade in response to DNA double-strand breaks (DSBs).

Autophagosome markers are molecular tools used to identify, localize autophagosomes and evaluate autophagic activity, serving as core components in studying autophagic mechanisms and analyzing autophagic abnormalities related to diseases.