Golgi

(Rac)-Golgicide A ((Rac)-GCA) is a racemate of Golgicide A, used in the synthesis of Golgicide A.

Golgicide A-1 (GCA-1) is a moderately potent cis-diastereomer variant of Golgicide A (GCA), designed specifically to inhibit mosquito reproduction.

Golgicide A-2 (GCA-2), a derivative of Golgicide A (GCA), is the highly active enantiomer of GCA. It exhibits exceptional selectivity and efficiency in eradicating An. stephensi larvae, making it valuable for dengue virus-related research.

Golgicide A is a potent and rapidly reversible GBF1 inhibitor.

Nigericin sodium salt is an antibiotic, an NLRP3 activator, and a cationic ion carrier. Nigericin sodium triggers the activation of the NALP3 inflammasome, which inhibits Golgi function and suppresses the growth of Gram-positive bacteria.

alphaSYN-IN-NAB2, a neuron-protective agent, is a protein encoded by the NAB2 gene. NAB2 effectively and selectively protects a variety of cells from alpha-SYN toxicity. NAB2 promotes endosomal transport dependent on E3 ubiquitin ligase Rsp5 Nedd4. NAB2 identifies a viable molecular node in alpha-SYN biology that corrects multiple aspects of its underlying pathology, including dysfunctional endosomes and endoplasmic reticulum to Golgi vesicles transport. NAB2 is involved in cellular processes such as cell differentiation, apoptosis and stress response, and can be used to study cancer, neurodevelopment and neuronal activity.

Ceramides Mixture, an endogenous ceramide, consists of hydroxy and non-hydroxy fatty acid-containing ceramides. It is involved in the regulation of cell cycle arrest, growth inhibition, and modulation of telomerase activity.

Hyaluronic acid sodium (Sodium Hyaluronate) is an anionic, nonsulfated glycosaminoglycan distributed widely throughout connective, epithelial, and neural tissues. It is unique among glycosaminoglycans in that it is nonsulfated, forms in the plasma membrane instead of the Golgi, and can be very large, with its molecular weight often reaching the millions. One of the chief components of the extracellular matrix, hyaluronic acid contributes significantly to cell proliferation and migration, and may also be involved in the progression of some malignant tumors.

PD 128042 (CI 976) is a potent, orally active, and selective ACAT inhibitor (IC50: 73 nM) as well as a lysophospholipid acyltransferase (LPAT) inhibitor. CI 976 inhibits Golgi-associated LPAT activity (IC50: 15 μM) and multiple membrane trafficking steps.

Fatostatin hydrobromide (Fatostatin A HBr) ia an inhibitor of sterol regulatory element binding protein (SREBP). It impairs the activation of SREBP-1 and SREBP-2.

Ceapin-A7, with an IC50 of 0.59 μM, selectively inhibits ATF6α signaling in response to ER stress. This compound is instrumental in investigating ATF6α's activation mechanism and its function in pathological conditions.

Fatostatin is a specific inhibitor of SREBP activation, it impairs the activation of SREBP-1 and SREBP-2. Fatostatin binds to SCAP (SREBP cleavage-activating protein), and inhibits the ER-Golgi translocation of SREBPs.

Retro-2 (2-{[(5-methyl-2-thienyl)methylene]amino}) is a plant toxin ricin inhibitor, itprotects HeLa cells against Ricin, Stx1 and Stx2, selectively blocks retrograde toxin trafficking at the early endosome-TGN (trans-Golgi network) interface.

ZCL278 is a selective Cdc42 GTPase inhibitor.

BML-265 is a potent inhibitor of EGFR tyrosine kinase (EGFR tyrosine kinase). It disrupts Golgi apparatus integrity in human cells and hinders the transport of secretory proteins across various substances. In contrast, BML-265 does not affect the integrity and transport of the Golgi apparatus in rodent cells.

D011-2120 is an agent of antiviral that acts by blocking microtubule polymerization, disrupting the Golgi complex and inhibiting viral trafficking to the plasma membrane during virus egress.

G202-0362 is an antiviral agent against Rift Valley fever virus. It acts by blocking virus budding from the trans Golgi.

Sulfatides are endogenous sulfoglycolipids with various biological activities in the central and peripheral nervous systems, pancreas, and immune system. They are produced from the combination of ceramide and UDP-galactose in the endoplasmic reticulum followed by sulfation in the Golgi apparatus. The ceramide portion contains variable fatty acid chain lengths, which are tissue- and pathology-dependent. Sulfatides are primarily found in the myelin sheath of oligodendrocytes and Schwann cells, with smaller chain lengths predominant during development and longer chain lengths predominant in mature cells. They accumulate in the lysosome of patients with metachromatic leukodystrophy, a disorder characterized by arylsulfatase A deficiency. Sulfatides are also located in pancreatic β-cells and inhibit insulin release from isolated rat pancreatic islet cells, suggesting a potential role in diabetes. Sulfatides can induce inflammation in glia in vitro and certain sulfatides, such as C24:1 3'-sulfo-galactosylceramide, can induce an immune response in vitro in mouse splenocytes. Sulfatides (bovine) (sodium salt) is a mixture of isolated bovine sulfatides.

Ceramide phosphoethanolamine (CPE) is an analog of sphingomyelin that contains ethanolamine rather than choline as the head group. It is the principal membrane phospholipid in invertebrates such as Drosophila, which lacks sphingomyelin. It is only produced in small amounts in mammalian cells, accounting for approximately 0.02 mol% of total phospholipids in mouse testis and brain. In Drosophila, CPE is biosynthesized by CPE synthase from ceramide and cytidine diphosphate-ethanolamine in the Golgi lumen. In mammals, it is biosynthesized by sphingomyelin synthase 2 (SMS2) in the plasma membrane and by sphingomyelin synthase-related protein (SMSr) in the endoplasmic reticulum (ER). In Drosophila, CPE has a role in glial ensheathment of axons. Disrupting CPE synthesis by depleting SMSr in vitro in mammalian cells leads to an accumulation of ER ceramides, which are then mislocalized to the mitochondria, inducing apoptosis. However, ceramide levels are not altered in transgenic mice lacking SMSr catalytic activity. CPEs (bovine) is a mixture of CPEs with variable N-acyl chain lengths.

Exo2 is a secretion inhibitor that cell-specifically disrupts the integrity of the trans-Golgi network (TGN) and interferes with the delivery of Shiga toxin to the endoplasmic lumen, and can be used to examine membrane trafficking in mammalian cells.

Pepsin is an endopeptidase that breaks down proteins into smaller peptides and amino acids that can be easily absorbed in the small intestine[1]. Pepsin is stable at pH ranges as high as pH 6. Above this pH, pepsin is rapidly irreversibly inactivated and elevation of pH of the reaction mixture to pH 8 results in complete inactivation of pepsin[2]. Pepsin has been posited to be a reliable biological marker of EER. An immunologic pepsin assay of combined sputum and saliva was determined to be 100% sensitive and 89% specific for detection of EER (based on pH-metry), and an enzymatic test of nasal lavage fluid (100% sensitivity and 92.5% specificity) demonstrated an increased incidence of EER in patients with chronic rhinosinusitis[3]. Cultured hypopharyngeal epithelial (FaDu) cells were exposed to human pepsin (0.1 mg mL) at pH 7.4 for either 1 hour or 12 hours at 37°C and both mitochondria and Golgi complexes were clearly damaged. This finding reveals a novel mechanism by which pepsin could cause cell damage, potentially even in nonacidic refluxate[4].

M-COPA is a golgi disruptor which inhibits cell surface expression of MET protein and the ADP-ribosylation factor 1 (Arf1) activation. M-COPA also inhibits angiogenesis through suppression of both VEGFR1 2 and nuclear factor-kappaB (NF-kappaB) signaling pathways.

NC03 is a PI4K2A inhibitor which decreases the PI4P pools in Golgi and endosomes.

CMP-Sialic acid (CMP-Neu5Ac) acts as an allosteric inhibitor of UDP-GlcNAc 2-epimerase, is a substrate for Golgi sialyltransferases, and is essential for the biosynthesis of sialic acid and its conjugates [1].