Cellular Localization IF (Immunofluorescence) is an experimental method based on immunofluorescence technology, used to observe the distribution of specific antigens within cells.

Cdc25 is a protein phosphatase responsible for dephosphorylating and activating cdc2, a crucial step in regulating the entry of all eukaryotic cells into mitosis (1). cdc25C is constitutively phosphorylated at Ser216 throughout interphase by c-TAK1, while phosphorylation at this site is DNA damage-dependent at the G2/M checkpoint (2). When phosphorylated at Ser216, cdc25C binds to members of the 14-3-3 family of proteins, sequestering cdc25C in the cytoplasm and thereby preventing premature mitosis (3). The checkpoint kinases Chk1 and Chk2 phosphorylate cdc25C at Ser216 in response to DNA damage (4,5).

c-Kit is a member of the subfamily of receptor tyrosine kinases that includes PDGF, CSF-1, and FLT3/flk-2 receptors. It plays a critical role in activation and growth in a number of cell types, including hematopoietic stem cells, mast cells, melanocytes, and germ cells.

CDK Cyclin-dependent kinases (CDKs) are the core effectors of cell cycle progression. CDK activity is regulated through association with their cyclin partners and cyclin-dependent kinase inhibitors (CKIs) as well as by activating and inhibitory phosphorylation events.

Cell fractionation is the process of separating cellular components, such as organelles, proteins, and other macromolecules, from the entire cell.

Animal development from a single-cell zygote to fertile adult requires many rounds of cell division. During each division, cells complete an ordered series of events that collectively form the "cell cycle".

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.