MYT1 (Phospho-Ser83) Antibody
- Known as:
- MYT1 (Phospho-Ser83) Antibody
- Catalog number:
- 11745
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- MYT1 (Phospho-Ser83) Antibody
Related genes to: MYT1 (Phospho-Ser83) Antibody
- Gene:
- MYT1 NIH gene
- Name:
- myelin transcription factor 1
- Previous symbol:
- PLPB1
- Synonyms:
- MTF1, MYTI, ZC2HC4A, NZF2, ZC2H2C1
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-08
- Date modifiied:
- 2019-02-07
- Gene:
- PKMYT1 NIH gene
- Name:
- protein kinase, membrane associated tyrosine/threonine 1
- Previous symbol:
- -
- Synonyms:
- MYT1, PPP1R126
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-20
- Date modifiied:
- 2014-11-19
Related products to: MYT1 (Phospho-Ser83) Antibody
Related articles to: MYT1 (Phospho-Ser83) Antibody
- Current therapy for advanced adrenocortical carcinoma (ACC) is represented by EDP-M (etoposide, doxorubicin, cisplatin + mitotane), but its efficacy is limited and new approaches are needed. Our previous in vitro findings showed that AZD1775, an inhibitor of the G2/M checkpoint gatekeeper Wee1, reduces proliferation and increases apoptosis in ACC cell models. The compensatory upregulation of Myt1, a Wee1-redundant kinase, has been involved in the onset of AZD1775 resistance in other tumour types. Aim of this study was to investigate in vitro and in vivo the effects of AZD1775 alone or combined with EDP-M, and to explore the onset of molecular mechanisms of resistance. In vitro experiments in human ACC cell line NCI-H295R demonstrated that coincubation of AZD1775 and EDP-M exerted synergistic effects in reducing cell viability and proliferation and additive effects in inhibiting cortisol secretion. In NCI-H295R xenografts in nude mice, AZD1775 demonstrated an antitumor efficacy comparable to EDP-M, without synergistic effects. Myt1 upregulation was observed after Wee1 silencing or inhibition by AZD1775 in NCI-H295R and patient-derived ACC cells, but not in mice tumours after 22-days treatment with AZD1775 and/or EDP-M. Interestingly, Myt1 increase after AZD1775 treatment in primary ACC cells was reverted by EDP-M cotreatment. Overall, our data in in vitro and in vivo preclinical ACC models support AZD1775 as a promising ACC therapeutic option, and its combination with EDP-M as a useful strategy to enhance drug efficacy, reduce cortisol secretion, prevent drug resistance and minimize side effects by reducing the therapeutic dosage. - Source: PubMed
Publication date: 2025/10/15
Nozza EmmaEsposito EmanuelaDi Muro GenesioDi Bari SoniaCatalano RosaLopez GianlucaVaira ValentinaBarbieri Anna MariaMarra GiusyMangili FedericaTreppiedi DonatellaBattistin MicheleDi Dalmazi GuidoPalmieri SerenaFerrante EmanueleMantovani GiovannaPeverelli Erika - Ataxia telangiectasia and Rad3-related (ATR) and checkpoint kinase 1 (Chk1) are crucial kinases in the DNA damage response (DDR) pathway. While the roles of ATR and Chk1 within the DDR are well established, their roles in mitosis are not fully understood. Here, we describe that the ATR-Chk1 pathway is rewired during mitosis to promote full CDK1 activity, starkly contrasting its role in interphase, where it inhibits CDK1 following DNA damage in human cells. In mitosis, Chk1 inhibits residual activity of PKMYT1 (Myt1) via direct phosphorylation at Serine 143. Partial loss of CDK1 activity caused by inhibition of mitotic Chk1 leads to different effects on mitotic progression than full CDK1 inhibition. It causes increased lagging chromosomes in part through loss of Aurora B activity. Thus, mitosis-specific ATR-Chk1 activity is necessary to promote faithful chromosome segregation by ensuring that CDK1 activity is maintained in mitosis. - Source: PubMed
Publication date: 2025/07/23
Joo Yoon KiParrado Carlos RamirezLi WenxueYang RanBlack ElizabethBleichert FranziskaLiu YanshengKabeche Lilian - Cell-cycle checkpoints are stringent quality control mechanisms that regulate cell-cycle progression and division. Cancer cells often develop a dependency on the G2-M cell-cycle checkpoint to facilitate DNA repair and resolve intrinsic or therapy-induced DNA damage. This dependency leads to therapy resistance, continuous cell division, and disease progression. Targeting G2-M checkpoints has been heavily pursued over the past two decades and has progressed into clinical studies. Recent genome-scale functional genomic studies have revealed that protein kinase, membrane-associated tyrosine/threonine 1, an essential but previously overlooked molecule for the G2-M checkpoint, is a promising target for multiple types of cancers. In this work, we summarize the latest discoveries in molecular targeting of protein kinase, membrane-associated tyrosine/threonine 1, and discuss the challenges and limitations in expanding its clinical application. - Source: PubMed
Lang FengchaoKaur KarambirZaheer JaveriaRibeiro Diego LuisYang Chunzhang - The cell cycle includes two checkpoint arrests allowing to repair of damaged DNA. Many cancer cell lines exhibit weak G1 checkpoint mechanisms relying significantly more on the G2 checkpoint than do healthy cells. Inhibition of Myt1 kinase (PKMYT1), a forgotten member of the Wee family, cyclin-dependent kinase 1 (Cdk1) inhibitory kinase, target for G2 checkpoint abrogation, whose inhibition forces cells into premature unchecked mitosis resulting in cell death, is a promising concept for anticancer therapy. There are not many inhibitors of this emerging, potentially clinically important kinase. Herein, the valuable insight into structural features and binding mechanisms of diaminopyrimidines, aminoquinolines, quinazolines, pyrido[2,3-d]pyrimidines, pyrazolo[3,4-d]pyrimidines, and pyrrolo[2,3-b]quinoxalines, as well as finally made a general scheme of fragmented structures of Myt1 inhibitors with the enzyme, offer potential frameworks useful for future directions, for further chemical optimizations, in the discovery and the design of novel effective structures, potential therapeutics. - Source: PubMed
Publication date: 2024/02/06
Tomović Pavlović KatarinaKocić GordanaŠmelcerović Andrija - The cell cycle is tightly regulated by checkpoints, which play a vital role in controlling its progression and timing. Cancer cells exploit the G2/M checkpoint, which serves as a resistance mechanism against genotoxic anticancer treatments, allowing for DNA repair prior to cell division. Manipulating cell cycle timing has emerged as a potential strategy to augment the effectiveness of DNA damage-based therapies. - Source: PubMed
Lang FengchaoCornwell James AKaur KarambirElmogazy OmarZhang WeiZhang MeiliSong HuaSun ZhongheWu XiaolinAladjem Mirit IAregger MichaelCappell Steven DYang Chunzhang