| Features: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Taurine (2-aminoethanesulfonic acid) is a sulfur-containing “amino acid–like” molecule (not incorporated into proteins). It’s abundant in many tissues and is best thought of as a homeostatic modulator rather than a direct cytotoxin.Core biology themes: -Osmoregulation / membrane stabilization -Mitochondrial support + anti-oxidant tone (indirect) -Calcium handling modulation -Anti-inflammatory signaling (context-dependent) -Bile acid conjugation (tauroursodeoxycholic-type physiology, but taurine itself is a conjugating substrate) Cancer relevance (preclinical/adjunct framing): -Often discussed as protective (normal-tissue protection) and stress-modulating, not a primary anti-cancer agent. -May influence redox balance, ER stress, and inflammation, which can indirectly affect tumor biology or therapy tolerance (model-dependent). -ROS axis: tends to reduce oxidative injury (indirect) -NRF2: sometimes reported as part of antioxidant adaptation, but not a “core direct target”Amino acid that benefits the heart, brain and immune system. Taurine, an organic compound containing sulfur in its chemical structure, possesses anti-inflammatory, anti-oxidant, and various physiological functions within the cardiovascular, kidney, endocrine, and immune systems. Also an LDH inhibitor -Neuroprotection: helps protect neurons against excitotoxicity (e.g., glutamate damage) and ROS stress. -Anti-oxidative action: scavenges ROS, reducing oxidative stress seen in AD brains. -Anti-inflammatory -Calcium homeostasis Helps maintain intracellular calcium balance, disrupted in AD. -Amyloid-beta toxicity May reduce Aβ-induced neurotoxicity and cell death in vitro. -Tau pathology: possible reduction of tau hyperphosphorylation. -Memory and cognition may improve learning and memory.
Time-Scale Flag (TSF): P / R / G
Alzheimer’s Disease (AD)-Oriented Time-Scale Flagged Pathway Table
Time-Scale Flag (TSF): P / R / G
|
| Source: |
| Type: |
| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 3950- | Taur, | Taurine Supplementation as a Neuroprotective Strategy upon Brain Dysfunction in Metabolic Syndrome and Diabetes |
| - | Review, | Diabetic, | NA | - | Review, | Stroke, | NA | - | Review, | AD, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:158 Target#:38 State#:% Dir#:4
wNotes=0 sortOrder:rid,rpid