Category: 63208-82-2

The p53 inactivators pifithrin-μ and pifithrin-α mitigate TBI-induced neuronal damage through regulation of oxidative stress, neuroinflammation, autophagy and mitophagy was written by Yang, Ling-Yu;Greig, Nigel H.;Tweedie, David;Jung, Yoo Jin;Chiang, Yung-Hsiao;Hoffer, Barry J.;Miller, Jonathan P.;Chang, Ke-Hui;Wang, Jia-Yi. And the article was included in Experimental Neurology in 2020.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

Traumatic brain injury (TBI) is one of the most common causes of death and disability worldwide. We investigated whether inhibition of p53 using pifithrin (PFT)-α or PFT-μ provides neuroprotective effects via p53 transcriptional dependent or -independent mechanisms, resp. TBI-induced impairments were mitigated by both PFT-α and PFT-μ. Double immunofluorescence staining similarly demonstrated that PFT-μ significantly increased HO-1 pos. neurons and mRNA expression in the cortical contusion region as well as decreased numbers of 4-hydroxynonenal (4HNE)-pos. cells. Levels of mRNA encoding for p53, autophagy, mitophagy, anti-oxidant, anti-inflammatory related genes and proteins were measured by RT-qPCR and immunohistochem. staining, resp. PFT-α, but not PFT-μ, significantly lowered p53 mRNA expression. Both PFT-α and PFT-μ lowered TBI-induced pro-inflammatory cytokines (IL-1β and IL-6) mRNA levels as well as TBI-induced autophagic marker localization (LC3 and p62). Finally, treatment with PFT-μ mitigated TBI-induced declines in mRNA levels of PINK-1 and SOD2. Our data suggest that both PFT-μ and PFT-α provide neuroprotective actions through regulation of oxidative stress, neuroinflammation, autophagy, and mitophagy mechanisms, and that PFT-μ, in particular, holds promise as a TBI treatment strategy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring has been identified as a central feature of numerous natural products, perhaps the most famous example of which is epothilone. The pyridine-type nitrogen in the thiazole ring deactivates the ring for electrophilic substitution reactions, which is further reduced in acid due to protonation of the thiazole ring.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Host Proteins Identified in Extracellular Viral Particles as Targets for Broad-Spectrum Antiviral Inhibitors was written by Gale, Trevor V.;Horton, Timothy M.;Hoffmann, Andrew R.;Branco, Luis M.;Garry, Robert F.. And the article was included in Journal of Proteome Research in 2019.HPLC of Formula: 63208-82-2 The following contents are mentioned in the article:

Liquid chromatog. mass spectrometry (LCMS) proteomic analyses have revealed that host proteins are often captured in extracellular virions. These proteins may play a role in viral replication or infectivity and can represent targets for broad-spectrum antiviral agent development. The authors utilized LCMS to determine the host protein composition of Lassa virus-like particles (LASV VLPs). Multiple host proteins incorporated in LASV VLPs are also incorporated in unrelated viruses, notably ribosomal proteins. The authors assembled a data set of host proteins incorporated into extracellular viral particles. The frequent incorporation of specific host proteins into viruses of diverse families suggests that interactions of these proteins with viral factors may be important for effective viral replication. Drugs that target virion-associated host proteins could affect the protein in the extracellular virion or the host cell. Compounds that target proteins incorporated into virions with high frequency, but with no known antiviral activity, were assayed in a scalable viral screening platform, and hits were tested in competent viral systems. One of these mols., GAPDH modulating small mol. CGP 3466B maleate (Omigapil), exhibited a dose-dependent inhibition of HIV, dengue virus, and Zika virus. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2HPLC of Formula: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The higher aromaticity of thiazole is due to delocalization of a lone pair of sulfur electrons across the ring, which is evidenced by chemical shifts of ring hydrogen at δ 7.27 and 8.77 ppm (C2 and C4), indicating diamagnetic ring current. Various laboratory methods exist for the organic synthesis of thiazoles. Prominent is the Hantzsch thiazole synthesis is a reaction between haloketones and thioamides.HPLC of Formula: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Mode of action of carboplatin via activating p53/miR-145 axis in head and neck cancers was written by Kilic, Ahsen;Barlak, Neslisah;Sanli, Fatma;Aytatli, Abdulmelik;Capik, Ozel;Karatas, Omer F.. And the article was included in Laryngoscope in 2020.Application In Synthesis of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

In this study, we aimed at investigating the expressions of miR-145 and its well-characterized direct targets on carboplatin treatment. The effect of carboplatin and miR-145 on the proliferative capacity of head and neck squamous cell carcinoma cells was evaluated using Cell Viability Detection Kit-8. Expressions of miR-145 and its targets were evaluated using quant. real-time polymerase chain reaction on carboplatin treatment and p53 inhibition. Western blot was used to measure the levels of p53 and its acetylated versions in cells treated with carboplatin and/or pifithrin-a. We demonstrated that carboplatin induced the expression of miR-145 in a dose-dependent manner and suppressed the expressions of miR-145 direct targets. In addition, we showed that inhibition of p53 by pifithrin-a in carboplatin-treated cells reduced miR-145 expression and reversed the suppression of miR-145 direct targets. Considering all these findings together, one of the proposed mechanisms of carboplatin to kill cells might be the induction of miR-145 and deregulation of its targets in parallel, via p53 activation, which happens through carboplatin’s DNA-damaging property. To the best of our knowledge, these findings are the first to reveal the relationship between carboplatin and miR-145 in cancer cells. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Application In Synthesis of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.Application In Synthesis of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Context-dependent regulation of immunoglobulin mutagenesis by p53 was written by Boettcher, Katrin;Braunschmidt, Kerstin;Hirth, Gianna;Schaerich, Karsten;Klassert, Tilman E.;Stock, Magdalena;Sorgatz, Janine;Fischer-Burkart, Sabine;Ullrich, Steffen;Frankenberger, Samantha;Kritsch, Daniel;Kosan, Christian;Kueppers, Ralf;Strobl, Lothar J.;Slevogt, Hortense;Zimber-Strobl, Ursula;Jungnickel, Berit. And the article was included in Molecular Immunology in 2021.Product Details of 63208-82-2 The following contents are mentioned in the article:

P53 plays a major role in genome maintenance. In addition to multiple p53 functions in the control of DNA repair, a regulation of DNA damage bypass via translesion synthesis has been implied in vitro. Somatic hypermutation of Ig genes for affinity maturation of antibody responses is based on aberrant translesion polymerase action and must be subject to stringent control to prevent genetic alterations and lymphomagenesis. When studying the role of p53 in somatic hypermutation in vivo, we found altered translesion polymerase-mediated A:T mutagenesis in mice lacking p53 in all organs, but notably not in mice with B cell-specific p53 inactivation, implying that p53 functions in non-B cells may alter mutagenesis in B cells. During class switch recombination, when p53 prevents formation of chromosomal translocations, we in addition detected a B cell-intrinsic role for p53 in altering G:C and A:T mutagenesis. Thus, p53 regulates translesion polymerase activity and shows differential activity during somatic hypermutation vs. class switch recombination in vivo. Finally, p53 inhibition leads to increased somatic hypermutation in human B lymphoma cells. We conclude that loss of p53 function may promote genetic instability via multiple routes during antibody diversification in vivo. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Product Details of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring has been identified as a central feature of numerous natural products, perhaps the most famous example of which is epothilone. The pyridine-type nitrogen in the thiazole ring deactivates the ring for electrophilic substitution reactions, which is further reduced in acid due to protonation of the thiazole ring.Product Details of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

P53 inhibition attenuates cisplatin-induced acute kidney injury through microRNA-142-5p regulating SIRT7/NF-κB was written by Chen, Guoxiao;Xue, Huanzhou;Zhang, Xiangsheng;Ding, Degang;Zhang, Shilong. And the article was included in Renal Failure in 2022.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

Renal tubular epithelial cell apoptosis is the main mechanism of cisplatin-induced acute kidney injury. The role of microRNAs (miRNAs) in the apoptosis of renal tubular epithelial cells has been suggested, but the underlying mechanism has not been fully elucidated. We used microarray anal. to identify miR-142-5p involved in cisplatin-induced acute kidney injury. miR-142-5p was down-regulated in human renal tubular epithelial (HK-2) cells with cisplatin treatment. Notably, the overexpression of miR-142-5p attenuated the cisplatin-induced HK-2 cell apoptosis and inhibition of miR-142-5p aggravated cisplatin-induced HK-2 cell apoptosis. During cisplatin treatment, p53 was activated. The inhibition of p53 by pifithrin-α attenuated the cisplatin-induced kidney injury and up-regulated miR-142-5p expression. We also identified the Sirtuin7 (SIRT7) as a target of miR-142-5p. Furthermore, we demonstrated that the inhibition of SIRT7 prevented cisplatin-induced HK-2 cell apoptosis and decreased the expression of nuclear factor kappa B (NF-KB). Our data revealed that p53 inhibition could attenuate cisplatin-induced acute kidney injury by up-regulating miR-142-5p to repress SIRT7/NF-KB. These findings may provide a novel therapeutic target of cisplatin-induced acute kidney injury. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). Various laboratory methods exist for the organic synthesis of thiazoles. Prominent is the Hantzsch thiazole synthesis is a reaction between haloketones and thioamides.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

P53/PANK1/miR-107 signalling pathway spans the gap between metabolic reprogramming and insulin resistance induced by high-fat diet was written by Yang, Lu;Zhang, Bin;Wang, Xinju;Liu, Zhenhua;Li, Juan;Zhang, Shumiao;Gu, Xiaoming;Jia, Min;Guo, Haitao;Feng, Na;Fan, Rong;Xie, Manjiang;Pei, Jianming;Chen, Li. And the article was included in Journal of Cellular and Molecular Medicine in 2020.Related Products of 63208-82-2 The following contents are mentioned in the article:

High-fat diet (HFD) leads to obesity, type II diabetes mellitus (T2DM) and increases the coincidence of cardiovascular diseases and cancer. Insulin resistance (IR) is considered as the ‘common soil’ of those diseases. Furthermore, people on HFD showed restrained glycolysis and enhanced fatty acid oxidation, which is the so-called metabolic reprogramming. However, the relationship between metabolic reprogramming and IR induced by HFD is still unclear. Here, we demonstrate that PANK1 and miR-107 were up-regulated in the liver tissue of mice on HFD for 16 wk and involved in metabolic reprogramming induced by palmitate acid (PA) incubation. Importantly, miR-107 within an intron of PANK1 gene facilitated IR by targeting caveolin-1 in AML12 cells upon PA incubation. Moreover, we identify that HFD enhanced P53 expression, and activation of P53 with nutlin-3a induced PANK1 and miR-107 expression simultaneously in transcriptional level, leading to metabolic reprogramming and IR, resp. Consistently, inhibition of P53 with pifithrin-α hydrobromide ameliorated PA-induced metabolic reprogramming and IR. Thus, our results revealing a new mechanism by which P53 regulate metabolism In addition, the results distinguished the different roles of PANK1 and its intron miR-107 in metabolic regulation, which will provide more accurate intervention targets for the treatment of metabolic diseases. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Related Products of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.Related Products of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

The COX-2 inhibitor NS398 selectively sensitizes hypoxic HeLa cells to ionising radiation by mechanisms both dependent and independent of COX-2 was written by Anoopkumar-Dukie, Shailendra;Conere, Tom;Houston, Aileen;King, Liam;Christie, David;McDermott, Catherine;Allshire, Ashley. And the article was included in Prostaglandins and Other Lipid Mediators in 2020.Reference of 63208-82-2 The following contents are mentioned in the article:

It is widely accepted that the hypoxic nature of solid tumors contribute to their resistance to radiation therapy. There is increasing evidence that cyclooxygenase-2 (COX-2) contributes to increased resistance of tumors to radiation therapy. Furthermore, the mechanism by which these agents act remain largely unclear. Therefore, the aim of this study was to determine the impact of COX-2 selective inhibitors on both normoxic and hypoxic radiosensitivity in vitro and the mechanisms underlying this. Because of the close, reciprocal relationship between COX-2 and p53 we investigated their contribution to radioresistance. To achieve this we exposed HeLa, MCF-7 and MeWo cells to the COX-2 selective inhibitor, NS398 (10μM). NS398 (10μM) selectively sensitized hypoxic HeLa and MCF-7 but not MeWo cells to ionising radiation (5 Gy). We also show that ionising radiation at 5 Gy results in phosphorylation of p53 at serine 15, a key phosphorylation site for p53-mediated apoptosis, and that hypoxia attenuates this phosphorylation. Attenuated phosphorylation of p53 under hypoxic conditions may therefore contribute to hypoxic radioresistance. We also show that NS398 selectively phosphorylates p53 under hypoxic conditions following irradiation at 5 Gy. p53 phosphorylation could be an underlying mechanism by which this agent and other COX-2 inhibitors sensitize tumors to radiation therapy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Reference of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole rings are planar and aromatic. Thiazoles are characterized by larger pi-electron delocalization than the corresponding oxazoles and have therefore greater aromaticity. Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.Reference of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Fabrication of a pH-responsive core-shell nanosystem with a low-temperature photothermal therapy effect for treating bacterial biofilm infection was written by Peng, Dan;Liu, Genhua;He, Ye;Gao, Pengfei;Gou, Shuangquan;Wu, Jing;Yu, Jinxiu;Liu, Peng;Cai, Kaiyong. And the article was included in Biomaterials Science in 2021.Formula: C16H19BrN2OS The following contents are mentioned in the article:

Recently, photothermal therapy (PTT) has been recognized as a viable alternative strategy against bacterial biofilm infection. However, the hyperthermia required for PTT to ablate a biofilm usually induces damage in normal tissues/organs nearby. Herein, we developed zeolite-based imidazole framework (ZIF-8)-coated mesoporous polydopamine (MPDA) core-shell nanoparticles and then loaded Pifithrin-μ (PES), a natural inhibitor of heat-shock protein (HSP) that plays an essential role in bacteria resisting heating-induced damage. The ZIF-8 shell of the MPDA@ZIF-8/PES nanoplatform enabled a rapid degradation in response to the acidic environment in bacterial biofilm infection, which triggered the controlled release of PES and Zn ions. As a result, HSP was remarkably suppressed for enhancing PTT efficacy upon mild near-IR light irradiation In addition, the release of Zn²⁺ also had an antibacterial/antibiofilm effect. Thus, the fabricated nanosystem was able to induce the effective elimination of the bacterial biofilm, realizing low-temperature PTT (~45 °C) with excellent antibacterial efficacy. This work presented here not only provides a facile approach to fabricate the MPDA@ZIF-8/PES nanosystem with the responsiveness of the bacterial infection environment, but also proposes a promising low-temperature PTT strategy to treat bacterial biofilm-infection effectively. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Formula: C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. Various laboratory methods exist for the organic synthesis of thiazoles. Prominent is the Hantzsch thiazole synthesis is a reaction between haloketones and thioamides.Formula: C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Triptolide enhances lipolysis of adipocytes by enhancing ATGL transcription via upregulation of p53 was written by Wang, Xiaoyu;Xu, Meixue;Peng, Ying;Naren, Qimuge;Xu, Yanting;Wang, Xin;Yang, Gongshe;Shi, Xin’E.;Li, Xiao. And the article was included in Phytotherapy Research in 2020.Recommanded Product: 63208-82-2 The following contents are mentioned in the article:

Lipolysis is an essential physiol. activity of adipocytes. The Patatin Like Phospholipase Domain Containing 2 (PNPLA2) gene encodes the enzyme adipose triglyceride lipase (ATGL) responsible for triglyceride hydrolysis, the first step in lipolysis. In this study, we investigated the potential of triptolide (TP), a natural plant extract, to induce weight loss by examining its effect on ATGL expression. We found that long- and short-term TP administration reduced body weight and fat weight and increased heat production in brown adipose tissue in wild-type C57BL/6 mice. In 3T3-L1 fibroblasts and porcine adipocytes, TP treatment reduced the number of lipid droplets as determined by Oil Red O and BODIPY staining, with concomitant increases in free fatty acid and triglyceride levels in the culture medium. Combined treatment with TP and p53 inhibitor reversed these lipolytic effects. We next amplified the ATGL promoter region and identified conserved p53 binding sites in the sequence by in silico anal. The results of the dual-luciferase reporter assay using a construct containing the ATGL promoter harboring the p53 binding site showed that p53 induces ATGL promoter activity and consequently, ATGL transcription. These results demonstrate that TP has therapeutic value as an anti-obesity agent and acts by promoting lipolysis via upregulation of p53 and ATGL transcription. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Recommanded Product: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities. Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.Recommanded Product: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

FOXO1 mediates hypoxia-induced G0/G1 arrest in ovarian somatic granulosa cells by activating the TP53INP1-p53-CDKN1A pathway was written by Li, Chengyu;Liu, Zhaojun;Wu, Gang;Zang, Ziyu;Zhang, Jia-Qing;Li, Xiaoxuan;Tao, Jingli;Shen, Ming;Liu, Honglin. And the article was included in Development (Cambridge, United Kingdom) in 2021.SDS of cas: 63208-82-2 The following contents are mentioned in the article:

The development of ovarian follicles constitutes the foundation of female reproduction The proliferation of granulosa cells (GCs) is a basic process required to ensure normal follicular development. However, the mechanisms involved in controlling GC cell cycle are not fully understood. Here, by performing gene expression profiling in the domestic pig (Sus scrofa), we showed that cell cycle arrest at G0/G1 phase is highly correlated with pathways associated with hypoxic stress and FOXO signalling. Specifically, the elevated proportion of GCs at the arrested G0/G1 phase was accompanied by increased nuclear translocation of FOXO1 under conditions of hypoxia both in vivo and in vitro. Furthermore, phosphorylation of 14-3-3 by the JNK kinase is required for hypoxia-mediated FOXO1 activation and the resultant G0/G1 arrest. Notably, a FOXO1 mutant without DNA-binding activity failed to induce G0/G1 arrest of GCs during hypoxia. Importantly, we identified a new target gene of FOXO1, namely TP53INP1, which contributes to suppression of the G1-S cell cycle transition in response to hypoxia. Furthermore, we demonstrated that the inhibitory effect of the FOXO1-TP53INP1 axis on the GC cell cycle is mediated through a p53-CDKN1A-dependent mechanism. These findings could provide avenues for the clin. treatment of human infertility caused by impaired follicular development. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2SDS of cas: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. The pyridine-type nitrogen in the thiazole ring deactivates the ring for electrophilic substitution reactions, which is further reduced in acid due to protonation of the thiazole ring.SDS of cas: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica