Pentachloropseudilin
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| Category | Antibiotics |
| Catalog number | BBF-03054 |
| CAS | 69640-38-6 |
| Molecular Weight | 331.41 |
| Molecular Formula | C10H4Cl5NO |
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Description
Pentachloropseudilin is produced by the strain of Actinoplanes A/15104. It has the effect of anti-gram-positive bacteria and tinea trichoderma.
Specification
| Synonyms | Antibiotic A 15104Y; A 15104Y; Phenol, 2,4-dichloro-6-(3,4,5-trichloro-2-pyrrolyl)-; IA2 |
| IUPAC Name | 2,4-dichloro-6-(3,4,5-trichloro-1H-pyrrol-2-yl)phenol |
| Canonical SMILES | C1=C(C=C(C(=C1C2=C(C(=C(N2)Cl)Cl)Cl)O)Cl)Cl |
| InChI | InChI=1S/C10H4Cl5NO/c11-3-1-4(9(17)5(12)2-3)8-6(13)7(14)10(15)16-8/h1-2,16-17H |
| InChI Key | FBRLLYYPGGXCKT-UHFFFAOYSA-N |
Properties
| Appearance | Crystal |
| Antibiotic Activity Spectrum | Gram-positive bacteria; Fungi |
| Boiling Point | 445.9°C at 760 mmHg |
| Melting Point | 126-130°C |
| Density | 1.733 g/cm3 |
| Solubility | Soluble in Chloroform, Methanol |
Reference Reading
1. Pentachloropseudilin Treatment Impairs Host Cell Invasion by Trypanosoma cruzi
Mylla Spirandelli da Costa, Bruna Cristina Borges, Isabella Teixeira Marques, Rayane Cristina de Oliveira, Thaise Lara Teixeira, Julia de Gouveia Santos, Claudio Vieira da Silva Chembiochem. 2022 Sep 16;23(18):e202200349. doi: 10.1002/cbic.202200349. Epub 2022 Aug 9.
Pentachloropseudilin (PClP) is a reversible and allosteric inhibitor of type 1 myosin. Here, we addressed the impact of PClP treatment of Trypanosoma cruzi and mammalian host cell on the parasite migration, cell adhesion and invasion. We observed that PClP was not toxic to either T. cruzi or host cell. Moreover, treatment of T. cruzi with PClP inhabited parasite motility, host cell adhesion and invasion. Treatment of host cell with PClP also impaired parasite invasion probably by decreasing lysosome migration to the entry site of the parasite. Therefore, PClP treatment impaired fundamental processes necessary for a successful T. cruzi infection.
2. Measurement of junctional tension in epithelial cells at the onset of primitive streak formation in the chick embryo via non-destructive optical manipulation
Valentina Ferro, Manli Chuai, David McGloin, Cornelis J Weijer Development. 2020 Feb 4;147(3):dev175109. doi: 10.1242/dev.175109.
Directional cell intercalations of epithelial cells during gastrulation has, in several organisms, been shown to be associated with a planar cell polarity in the organisation of the actin-myosin cytoskeleton and is postulated to reflect directional tension that drives oriented cell intercalations. We have characterised and applied a recently introduced non-destructive optical manipulation technique to measure the tension in individual epithelial cell junctions of cells in various locations and orientations in the epiblast of chick embryos in the early stages of primitive streak formation. Junctional tension of mesendoderm precursors in the epiblast is higher in junctions oriented in the direction of intercalation than in junctions oriented perpendicular to the direction of intercalation and higher than in junctions of other cells in the epiblast. The kinetic data fit best with a simple viscoelastic Maxwell model, and we find that junctional tension, and to a lesser extent viscoelastic relaxation time, are dependent on myosin activity.
3. Myosin 1c: A novel regulator of glucose uptake in brown adipocytes
Alice Åslund, Muhammad Hamza Bokhari, Erika Wetterdal, René Martin, Hans-Joachim Knölker, Tore Bengtsson Mol Metab. 2021 Nov;53:101247. doi: 10.1016/j.molmet.2021.101247. Epub 2021 May 7.
Objective: The potential of brown adipose tissue (BAT) to influence energy homeostasis in animals and humans is encouraging as this tissue can increase fatty acid and glucose utilization to produce heat through uncoupling protein 1 (UCP1), but the actual mechanism of how the cell regulates glucose uptake is not fully understood. Myosin 1c (Myo1c) is an unconventional motor protein involved in several cellular processes, including insulin-mediated glucose uptake via GLUT4 vesicle fusion in white adipocytes, but its role in glucose uptake in BAT has not previously been investigated. Methods: Using the specific inhibitor pentachloropseudilin (PClP), a neutralizing antibody assay, and siRNA, we examined the role of Myo1c in mechanisms leading to glucose uptake both in vitro in isolated mouse primary adipocytes and in vivo in mice. Results: Our results show that inhibition of Myo1c removes insulin-stimulated glucose uptake in white adipocytes, while inducing glucose uptake in brown adipocytes, independent of GLUT4, by increasing the expression, translation, and translocation of GLUT1 to the plasma membrane. Inhibition of Myo1c leads to the activation of PKA and downstream substrates p38 and ATF-2, which are known to be involved in the expression of β-adrenergic genes. Conclusions: Myo1c is a PKA repressor and regulates glucose uptake into BAT.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
