PLK4 antibody
- Known as:
- PLK4 (anti-)
- Catalog number:
- orb100623
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PLK4 antibody
Related genes to: PLK4 antibody
- Gene:
- PLK4 NIH gene
- Name:
- polo like kinase 4
- Previous symbol:
- STK18
- Synonyms:
- Sak
- Chromosome:
- 4q28.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-09
- Date modifiied:
- 2016-01-22
Related products to: PLK4 antibody
Related articles to: PLK4 antibody
- Polo-like kinase 4 (PLK4), a master regulator of centrosome duplication, has emerged as an attractive therapeutic target in oncology. Notably, the synthetic lethality between PLK4 inhibition and amplification provides a strong rationale for targeted tumor intervention. However, the limited structural diversity of current PLK4 inhibitors constrains further development. Herein, structure-guided scaffold-hopping and fragment growth strategies were employed to develop a series of structurally novel quinazoline-based PLK4 inhibitors. The optimized compound () exhibited potent PLK4 inhibition (IC = 1.1 nM), excellent selectivity over Aurora A kinase (over 1600-fold), and favorable ADME and pharmacokinetic properties, including an oral bioavailability of 55.4%. further demonstrated significant in vitro and in vivo antitumor activity against -amplified neuroblastoma with a favorable safety profile. Overall, represents a promising lead for PLK4 inhibition, and offers new opportunities for precision therapy in -amplified neuroblastoma. - Source: PubMed
Publication date: 2026/07/16
Liu NianQi ZehuiSun WenqiangTong MinghuiShi XuanWang HanMu ShuyiHu NingyuanLuo ZiruiFan CunzhengZhang HaoyuGao ZixuanSun YinZhao DongmeiCheng Maosheng - Sinonasal squamous cell carcinoma (SNSCC) is a rare malignancy arising de novo or from inverted papilloma (IP), a benign neoplasm with malignant potential. The molecular drivers of IP-associated SNSCC (IP-SNSCC) remain poorly defined, and no effective therapies are available. Progress is hindered by limited preclinical studies and prospective clinical investigations. We performed multi-omic profiling, including whole-exome, RNA, and mitochondrial DNA sequencing (mtDNA-Seq), of matched normal sinonasal epithelium, IP, and SNSCC samples from 11 patients. Analyses revealed a stepwise transcriptional continuum across histological stages, marked by progressive activation of the cell cycle, extracellular matrix remodeling, and metabolic pathways, with suppression of immune and apoptotic signaling. Shared genomic aberrations were detected in only a subset of paired IP and SNSCC specimens, whereas mtDNA-Seq revealed no overlapping mutations, indicating divergent mitochondrial evolution even in clonally related lesions. Given the need for targeted therapies, we applied PandaOmics, an AI-driven target discovery platform, to genes progressively upregulated during IP-SNSCC development. We first prioritized targets with FDA-approved inhibitors, identifying CDK6, EGFR, HDAC, and SRC/YES1 as repurposing candidates, and nominated AURKA, PLK4, TTK, and CDK1/7 as druggable preclinical targets. Together, this study defines the molecular basis of IP-SNSCC and provides a foundation for future translational investigation. - Source: PubMed
Publication date: 2026/07/10
Singh AlkaKorzinkin MichaelSarkisova ViktoriaVergasova EkaterinaRosenberg Ari JSuresh KarthikMishra VasudhaMiao YuxuanShen LeSmolik JuliaVeviorskiy AlexanderPun Frank WCheng XiangyingWing ClaudiaPinto JayantLow Christopher MLingen Mark WRooper LisaPearson Alexander TVokes Everett ELiu XuanyaoLondon NyallZhavoronkov AlexAgrawal NishantIzumchenko Evgeny - Multipolar mitotic spindles with extra centrosomes, first observed in cancer cells in the late nineteenth century, remain poorly understood. Here, to address how cells overcome proliferation arrest imposed by centrosome amplification, we describe a genome-wide screen revealing that downregulation of the Wnt, Hippo, Tpr53, PIDDosome, ciliary biogenesis, or autophagy pathways enables proliferation of mouse embryonic stem cells having PLK4-mediated centrosome amplification. We select the tumor suppressor, Guanine-nucleotide Activating Protein ARHGAP15, for further study as its depletion activates autophagy, overcomes centrosome amplification, and enables embryonic fibroblast proliferation. Reduction of centrosomes following ARHGAP15 depletion requires autophagy protein, ATG16L1, which associates with ARHGAP15 when the autophagy pathway is inactive. ARHGAP15 is opposed by Guanine-nucleotide Exchange Factor ARHGEF2, which is activated by the centriolar protein CEP170 to generate RAC1-GTP and promote autophagy. Together our findings add extra dimensions to the roles of RAC1 in cytoskeletal regulation and ARHGAP15 as a potential tumor suppressor. - Source: PubMed
Publication date: 2026/06/21
Coelho Paula AFatalska AgnieszkaGeymonat MarcoLattao RamonaGlover David M - Polo-like kinase 4 (PLK4) is a key regulator of centriole duplication and contributes to mitotic spindle organization during cell division. PLK4 has been implicated as pharmacological target in a subset of breast cancers and neuroblastomas harboring 17q chromosomal gains and overexpression of the E3 ubiquitin-protein ligase TRIM37. Here, we investigated factors that influence sensitivity of cancer cells to PLK4 inhibition. - Source: PubMed
Publication date: 2026/06/18
Stoyanov MiroslavAquino-Perez CeciliaMazumder ShreyasiSalcakova DominikaPetrezselyova SilviaMacurek Libor - It was recently shown that inhibition of polo-like kinase 4 (PLK4) induces synthetic lethality in cancers with chromosome 17q-encoded TRIM37 copy number gain due to cooperative regulation of centriole duplication and mitotic spindle nucleation. We show here that chromosome 17q/TRIM37 gain is a defining feature of high-risk neuroblastoma and renders patient-derived cell lines hypersensitive to the novel PLK4 inhibitor RP-1664. We demonstrate that centriole amplification at low doses of RP-1664 contributes to this sensitivity in a TRIM37-independent fashion. CRISPR screens and live cell imaging reveal that upon centriole amplification, neuroblastoma cells succumb to multipolar mitoses due to an inability to cluster or inactivate supernumerary centrosomes. RP-1664 monotherapy showed robust anti-tumor activity in 14/15 human neuroblastoma-derived xenograft models, and significantly extended survival in a transgenic MYCN-driven murine model of neuroblastoma. RP-1664 combined with GD2-directed chemoimmunotherapy resulted in maintained complete responses in 6/9 mice with established MYCN-driven murine neuroblastomas. These data support clinical development of PLK4 inhibitors for high-risk neuroblastoma and other cancers with somatically acquired TRIM37 overexpression. - Source: PubMed
Publication date: 2026/06/13
Soria-Bretones IsabelCasás-Selves MatiasSamanta MinuGroff DavidMurray JayneFletcher Jamie IFarrel AlvinPastor StevenPatel KhushbuGoodfellow ElliotLi LiCaron CathyShiwram AriyaKim HyeyeonHenry DanielleLaterreur NancyBowlan JulianKrytska KaterynaNeuhauser Steven BStearns Timothy MSchubert Jeffrey AWu JinhuaSurrey Lea FMartinez DanielMak CrystalBrand JenniferWesley CaitlinSomers KlaartjeÁlvarez-Quilón AlejandroVallée FrédéricNejad ParhamSchonhoft Joseph DLi JoannaVeloso ArturYoung Jordan T FHyer Marc LMorris Stephen JMossé Yael PMarshall C GaryHaber MichelleZimmermann MichalMaris John M