Category: 321673-30-7

Tomlinson, Matthew L. published the artcileXenopus as a model organism in developmental chemical genetic screens, Name: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Molecular BioSystems (2005), 1(3), 223-228, database is CAplus and MEDLINE.

Chem. genetics is a potentially powerful tool for studying developmental processes in vertebrate systems. The authors present data showing X. laevis as a model organism in which systematic chem. genetic screens can be carried out. Previous forward chem. genetic screens, including those with developing zebrafish embryos, have demonstrated the nature and value of biol. information gained with this approach. The authors show how amenable Xenopus is to chem. genetics by investigating a series of compounds either with known biochem. effects, or previously identified to give developmental phenotypes, on a range of biol. functions, including the development of pigmentation, the heart, and the central nervous system in zebrafish. The authors have found that the compounds give comparable phenotypes when applied to developing Xenopus embryos. The authors have also studied the penetrance and expressivity of these chem. genetic phenotypes in relation to genetic variation and the developmental window during which the compound is present. Finally, the authors assess the feasibility and the potential throughput of a screen in this vertebrate species.

Molecular BioSystems published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C5H10Cl3O3P, Name: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Wong, Anthony published the artcileTissue-Reparative Benefits of MST1/2 Inhibition: Separating the Wheat From the Chaff, Product Details of C12H23N3S, the publication is Circulation Research (2021), 129(10), 927-929, database is CAplus and MEDLINE.

Identifying potential therapeutic targets for tissue repair following injury such as myocardial infarction (Ml) is a difficult task given the need to maintain the temporal balance of acute inflammation and resolution post-MI. Using XMU-MP-1 to inhibit MST1/2 activity, they found increased tissue fibrosis, left ventricular dilation, tissue fibrosis, inflammatory cytokine production, mortality, and decreased cardiac function. Importantly, pharmacol. inhibition of LTB4 alone had no effect, but when combined with XMU-MP-1 treatment, blockade of both MST1/2 and LTB4 ameliorated cardiac function and adverse tissue remodeling post-MI.

Circulation Research published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C13H14BNO2, Product Details of C12H23N3S.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Vincent, Christelle published the artcile5-LOX, 12-LOX and 15-LOX in immature forms of human leukemic blasts, Application In Synthesis of 321673-30-7, the publication is Leukemia Research (2008), 32(11), 1756-1762, database is CAplus and MEDLINE.

Several reports have demonstrated an important role of leukotriene B₄ (LTB₄) in the immune system. We investigated whether leukemic blasts from acute myeloid leukemic (AML) and acute lymphoid leukemic (ALL) patients produced LTB₄, 12- and 15-hydroxyeicosatetraenoic acids (12-HETE and 15-HETE) and whether these compounds affected blast proliferation and apoptosis. Leukemic blasts from AML M_0-2 and ALL patients expressed 5-LOX, 12-LOX and 15-LOX transcripts. Quant. polymerase chain reaction indicated that 5-LOX transcripts were far more abundant than 12-LOX and 15-LOX ones. Leukemic blasts expressed 5-LOX activating protein (FLAP) transcripts and produced LTB₄ in response to calcium ionophore. In contrast no 15-HETE production was found. Calcium ionophore-stimulated leukemic blasts produced 12-HETE but also released thromboxane A₂ suggesting that contaminating platelets accounted for the release of these compounds No significant effect of LTB₄, 12-HETE or 15-HETE could be documented on leukemic blast growth and on their apoptose rate. Results of the present study indicate that immature form of leukemic blasts produce LTB₄. However, the three major lipoxygenase metabolites of arachidonic acid; i.e., LTB₄, 12-HETE or 15-HETE, had no evident effect on their growth and apoptosis. We may speculate that LTB₄-derived blast cells might initiate, augment or prolong tissue inflammation and damages by affecting the marrow and blood cytokine network.

Leukemia Research published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C14H20BNO4, Application In Synthesis of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Wang, Meng published the artcileDifferential contribution of BLT1 and BLT2 to leukotriene B4-induced human NK cell cytotoxicity and migration, Related Products of amides-buliding-blocks, the publication is Mediators of Inflammation (2015), 389849/1-389849/14, database is CAplus and MEDLINE.

Accumulating evidence indicates that leukotriene B4 (LTB4) via its receptors BLT1 and/or BLT2 (BLTRs) could have an important role in regulating infection, tumor progression, inflammation, and autoimmune diseases. In the present study, we showed that LTB4 not only augments cytotoxicity by NK cells but also induces their migration. We found that approx. 30% of fresh NK cells express BLT1, 36% express BLT2, and 15% coexpress both receptors.The use of selective BLTR antagonists indicated that BLT1 was involved in both LTB4-induced migration and cytotoxicity, whereas BLT2 was involved exclusively in NK cell migration, but only in response to higher concentrations of LTB4. BLT1 and BLT2 expression increased after activation of NK cells with IL-2 and IL-15.These changes of BLTR expression by cytokines were reflected in enhanced NK cell responses to LTB4. Our findings suggest that BLT1 and BLT2 play differential roles in LTB4-induced modulation of NK cell activity.

Mediators of Inflammation published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C5H5F3O2, Related Products of amides-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Pernet, Erwan published the artcileLeukotriene B₄-type I interferon axis regulates macrophage-mediated disease tolerance to influenza infection, Quality Control of 321673-30-7, the publication is Nature Microbiology (2019), 4(8), 1389-1400, database is CAplus and MEDLINE.

Host defense against influenza A virus (IAV) infection depends not only on host resistance to eliminate the virus, but also disease tolerance to limit lung tissue damage and maintain pulmonary function. Fatal IAV infections are frequently the result of a maladaptive immune response that compromises disease tolerance rather than host resistance to infection. Here, we show that the leukotriene B₄ (LTB₄)-type I interferon (IFN) axis promotes a distinct mechanism of disease tolerance to pulmonary IAV infection. We demonstrate that mice genetically deficient in LTB₄ signalling (Blt1R^-/-) are more susceptible to IAV infection compared to control mice, despite similar pulmonary viral loads. The increased susceptibility of Blt1R^-/- mice is associated with an accumulation of inflammatory monocyte-derived macrophages (IMMs) causing increased lung immunopathol. We mechanistically define that LTB₄ signalling via the BLT1 receptor enhances the activation of the type I IFN-α/β receptor (IFNAR)/ and signal transducer and activator of transcription 1 (STAT1), which leads to IFN-α production by interstitial macrophages to suppresse in situ IMM proliferation. Importantly, the delivery of a single dose of LTB₄ at the peak viral load reduces IMM proliferation, controls tissue damage and increases survival without affecting host resistance to IAV.

Nature Microbiology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Quality Control of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Emre, Ceren published the artcileAge-related changes in brain phospholipids and bioactive lipids in the APP knock-in mouse model of Alzheimers disease, Application In Synthesis of 321673-30-7, the publication is Acta Neuropathologica Communications (2021), 9(1), 116, database is CAplus and MEDLINE.

Sustained brain chronic inflammation in Alzheimers disease (AD) includes glial cell activation, an increase in cytokines and chemokines, and lipid mediators (LMs), concomitant with decreased pro-homeostatic mediators. The inflammatory response at the onset of pathol. engages activation of pro-resolving, pro-homeostatic LMs followed by a gradual decrease. We used an APP knock-in (App KI) AD mouse that accumulates β-amyloid (Aβ) and presents cognitive deficits (at 2 and 6 mo of age, resp.) to investigate LMs, their precursors, biosynthetic enzymes and receptors, glial activation, and inflammatory proteins in the cerebral cortex and hippocampus at 2-, 4-, 8- and 18-mo-old in comparison with wild-type (WT) mice. We used LC-mass-spectrometry and MALDI mol. imaging to analyze LMs and phospholipids, and immunochem. for proteins. Our results revealed an age-specific lipid and cytokine profile, and glial activation in the App KI mice. Despite an early onset of Aβ pathol., pro-inflammatory and pro-resolving LMs were prominently increased only in the oldest age group. Furthermore, the LM biosynthetic enzymes increased, and their receptor expression decreased in the aged App KI mice. Arachidonic acid (AA)-containing phospholipid mol. species were elevated, correlating with decreased cPLA2 activity. MALDI mol. imaging depicted differential distribution of phospholipids according to genotype in hippocampal layers. Brain histol. disclosed increased microglia proliferation starting from young age in the App KI mice, while astrocyte numbers were enhanced in older ages. Our results demonstrate that the brain lipidome is modified preferentially during aging as compared to amyloid pathol. in the model studied here. However, alterations in phospholipids signal early pathol. changes in membrane composition

Acta Neuropathologica Communications published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Application In Synthesis of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Zhang, Shui-Juan published the artcileIntracerebroventricular injection of leukotriene B₄ attenuates antigen-induced asthmatic response via BLT1 receptor stimulating HPA-axis in sensitized rats, Synthetic Route of 321673-30-7, the publication is Respiratory Research (2010), No pp. given, database is CAplus and MEDLINE.

Basic and clin. studies suggest that hypothalamic-pituitary-adrenal (HPA) axis is the neuroendocrine-immune pathway that functionally regulates the chronic inflammatory disease including asthma. Our previous studies showed corresponding changes of cytokines and leukotriene B₄ (LTB₄) between brain and lung tissues in antigen-challenged asthmatic rats. Here, we investigated how the increased LTB₄ level in brain interacts with HPA axis in regulating antigen-induced asthmatic response in sensitized rats. Ovalbumin-sensitized rats were challenged by inhalation of antigen. Rats received vehicle, LTB₄ or U75302 (a selective LTB₄ BLT1 receptor inhibitor) was given via intracerebroventricular injection (i.c.v) 30 min before challenge. Lung resistance (R_L) and dynamic lung compliance (C_dyn) were measured before and after antigen challenge. Inflammatory response in lung tissue was assessed 24 h after challenge. Expression of CRH mRNA and protein in hypothalamus were evaluated by RT-PCR and Western Blot, and plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT) were measured using the ELISA kits. Antigen challenge decreased pulmonary function and induced airway inflammation, evoked HPA axis response in sensitized rats. Administration of LTB₄ via i.c.v markedly attenuated airway contraction and inflammation. Meanwhile, LTB₄ via i.c.v markedly increased CORT and ACTH level in plasma before antigen challenge, and followed by further increases in CORT and ACTH levels in plasma after antigen challenge in sensitized rats. Expression of CRH mRNA and protein in hypothalamus were also significantly increased by LTB₄ via i.c.v in sensitized rats after antigen challenge. These effect were completely blocked by pre-treatment with BLT1 receptor antagonist U75302 (10 ng), but not by BLT2 antagonist LY255283. LTB₄ administered via i.c.v down-regulates the airway contraction response and inflammation through activation of the HPA axis via its BLT1 receptor. This study expands our concept of the regulatory role of intracranial inflammatory mediators in inflammatory diseases including asthma. The favorable effects of LTB₄ on the HPA axis may help to explain the phenomenon of self-relief after an asthmatic attack.

Respiratory Research published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C8H7ClO3, Synthetic Route of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Kheradmand, Farrah published the artcileLeukotriene A₄ hydrolase: the janus enzyme shows its ugly side in smokers, Synthetic Route of 321673-30-7, the publication is American Journal of Respiratory and Critical Care Medicine (2014), 190(1), 5-7, database is CAplus and MEDLINE.

This paper describes the cigarette smoke chem. acetylates proline-glycine-proline, enhancing its chemotactic activity and protecting it from degradation by LTA4H. And also biochem. and preliminary murine studies suggest that cigarette smoke can selectively abrogate the peptidase activity of LTA4H, with minimal effect on the hydrolase activity.

American Journal of Respiratory and Critical Care Medicine published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Synthetic Route of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Sahoo, Daisy published the artcileScavenger receptor class B Type I (SR-BI) assembles into detergent-sensitive dimers and tetramers, Name: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids (2007), 1771(7), 807-817, database is CAplus and MEDLINE.

High d. lipoproteins (HDL) are protective against cardiovascular disease due to their important role in the reverse cholesterol transport (RCT) pathway. The selective transfer of cholesteryl ester (CE) from the HDL core to cells, the last step in RCT, is mediated by scavenger receptor class B type I (SR-BI). SR-BI is a heavily glycosylated cell surface receptor that is highly expressed in the liver, ovaries, testes and adrenal glands, where selective uptake of HDL-CE is most prevalent. Previous studies have shown that SR-BI oligomerizes with itself in steroidogenic tissues as well as in diverse cell lines. In the present study, we provide further evidence for the homo-oligomerization of SR-BI. We show by FPLC and blue native PAGE that SR-BI forms complexes whose sizes suggest the formation of monomers, dimers, and tetramers. Interestingly, homo-oligomerization occurs even with the absence of SR-BI’s C-terminal cytoplasmic domain. Finally, we report that an inhibitor of SR-BI-mediated cholesterol transport, BLT-1, and mutations in the putative leucine zipper region of SR-BI have profound effects on SR-BI function, however, they do not affect receptor self-association These observations indicate that SR-BI homo-oligomerization occurs even when the receptor is non-functional.

Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Name: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Hansen, Trond Vidar published the artcileThe novel lipid mediator PD1_n-3 DPA: An overview of the structural elucidation, synthesis, biosynthesis and bioactions, Related Products of amides-buliding-blocks, the publication is Prostaglandins and Other Lipid Mediators (2017), 103-110, database is CAplus and MEDLINE.

A review. Resolvins, protectins and maresins are individual families of specialized pro-resolving mediators biosynthesized from the dietary n-3 polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid. These enzymically oxygenated polyunsaturated lipid mediators were first elucidated during the resolution phase of acute inflammation in animal models of self-limited inflammation. Specialized pro-resolving mediators display potent bioactions when administrated in vivo. Biosynthetic pathway studies have revealed that individual lipoxygenases and cyclooxygenase-2 converts eicosapentaenoic acid and docosahexaenoic acid into distinct families of the resolvins, protectins and maresins. Recently n-3 docosapentaenoic acid was found to be a substrate for the biosynthesis of several novel families of specialized pro-resolving mediators. One example is PD1_n-3 DPA. During the 6th European Workshop on Lipid Mediators, Frankfurt, Germany, the structural elucidation, total organic synthesis, studies on the biosynthetic pathway, as well as the potent anti-inflammatory and pro-resolving properties of PD1_n-3 DPA were presented. Herein, we provide an overview of these topics for the new member PD1_n-3 DPA of the super-family of pro-resolving mediators.

Prostaglandins and Other Lipid Mediators published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Related Products of amides-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics