CDK4_RAT Cdk4 ELISA tesk kit
- Known as:
- CDK4_RAT Cdk4 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15861
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CDK4_RAT Cdk4 ELISA tesk kit
Related genes to: CDK4_RAT Cdk4 ELISA tesk kit
- Gene:
- CDK4 NIH gene
- Name:
- cyclin dependent kinase 4
- Previous symbol:
- -
- Synonyms:
- PSK-J3
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-28
- Date modifiied:
- 2019-04-23
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- Fine particulate matter (PM) exposure increases the risk of neurodevelopmental abnormalities by disrupting neural stem cell (NSC) proliferation and cell cycle homeostasis, which are critical for normal neurodevelopment. This study investigated the impact of fine particulate matter (PM) on NSC proliferation and cell cycle using a three-dimensional (3D) graphene oxide (GO) scaffold that mimics the NSC microenvironment. PM exposure led to concentration-dependent decreases in NSC viability and induced G0/G1 phase arrest via the marked downregulation of Cyclin D1-Cdk4 and Cyclin E-Cdk2, which critically impact G1/S transition. NSCs in 3D GO scaffolds maintained higher expression of key cell cycle regulators (Cyclin A, Cdk1/Cdk2, APC, and Cdc20) and superior cell viability when suffering PM exposure, demonstrating the 3D culture environment was beneficial for NSC proliferation. We speculate that the 3D culture environment is more favorable and protective for cell proliferation. Therefore, these findings highlight the utility of the 3D GO scaffold for studying PM effects on growing neural stem cells. This work provides a physiologically relevant in vitro platform that captures microenvironment-dependent neurotoxic responses, consequently offering valuable mechanistic insights into PM-induced developmental neurotoxicity. - Source: PubMed
Publication date: 2026/06/21
Li SiqiChang HuiyunGao MengjieZhang WenlouDeng FurongChen FenggeZhu XiaomanSong YuZhang HongLiu ShaojieMu YingMa HuiZhang Ying - Extrachromosomal DNA (ecDNA) amplification represents a distinct mechanism of genomic instability in cancer, increasingly recognized for its role in aggressive disease progression. This review examines how ecDNA drives tumour evolution and assesses its potential as both a prognostic marker and therapeutic target. - Source: PubMed
Publication date: 2026/06/12
Gajewski FilipPec JoannaKleinrok JakubPająk WeronikaPacyna KatarzynaTokarzewska AgataKrawczyk Paweł - Germline BRCA1/2-mutated (gBRCAm) hormone receptor-positive/HER2-negative (HR+/HER2-) metastatic breast cancer (MBC) is a biologically distinct subset in which the efficacy of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors remains incompletely characterized. We evaluated real-world outcomes and prognostic factors in a multicenter retrospective Turkish cohort treated with a CDK4/6 inhibitor plus endocrine therapy (June 2020-September 2025). Progression-free survival (PFS) and overall survival (OS) were estimated using Kaplan-Meier and Cox methods. Among 121 patients, 30 (24.8%) had BRCA1, 88 (72.7%) had BRCA2, and three (2.5%) had dual mutations; 66.9% received first-line therapy, with ribociclib in 69.4% and palbociclib in 29.8%. Objective response rate was 69.4% and the clinical benefit rate was 82.6%. Median PFS was 17.0 months and OS 47.0 months. PFS was numerically longer in BRCA1 than in BRCA2 carriers (25.0 vs. 14.0 months), although the difference was not statistically significant in the pairwise comparison (HR 1.50, 95% CI 0.88-2.56; log-rank = 0.135); the dual BRCA1/2 subgroup ( = 3) had the poorest outcomes and was assessed descriptively. OS did not differ significantly between BRCA1 and BRCA2 carriers (57.0 vs. 49.0 months; log-rank = 0.520). PFS did not differ between ribociclib and palbociclib ( = 0.192); OS favored ribociclib at borderline significance ( = 0.050), but this was not confirmed in Cox regression. In multivariable analysis, ECOG ≥ 1 (HR 1.85; = 0.010) and fulvestrant-based therapy (HR 1.74; = 0.041) predicted shorter PFS; fulvestrant also predicted worse OS (HR 2.39; = 0.008). CDK4/6 inhibitor-based therapy shows meaningful activity in gBRCAm HR+/HER2- MBC; the numerically poorer outcomes observed in BRCA2 carriers are hypothesis-generating and warrant validation in larger cohorts. - Source: PubMed
Publication date: 2026/06/17
Seyyar MustafaKalem AliSali MürselKarabuğa BerkanSahin Taha KorayDişli Ahmet KürşadTürkel AlperKaradurmuş BerkanŞahin Hafızoğlu EceAvcı NilüferBilgetekin IremKöse Baytemur NaziyetUguztemur EsmaOflazoğlu UtkuGür Hasibe BilgeHacıbekiroğlu İlhanAkkuş Aysun FatmaTopaloğlu SernazBayramgil AyberkDülgar Kaya ÖzgecanYazıcı MelikeŞakalar TeomanAkay SevalMajidova NargizGuliyev MuradAlan ÖzkanGülcü SerkanEren Tülayİmamoğlu Gökşen İnançGüren Ali KaanKöstek OsmanÜnlü AhmetOzturk BanuAydın EsraSafarov ShamkhalDoğan BekirTükenmez Mehmet AkifDemir TeyfikŞahin ElifErdemoğlu EnginKeskin Uzundere FatmaBütün OsmanKarabulut BülentUzun MehmetBaydaş TubaKaraman ElanurArak HacıEkinci FerhatAykan Musa BarışErtürk İsmailGuven Deniz CanDeligönül AdemKaraçin CengizAteş Öztürkİnanç MevlüdeYeşil HavvaAksoy SercanKöşeci TolgaÖkten İlker NihatYıldırım Hasan ÇağrıÇabuk Devrim - https://bit.ly/48nGZ3t. - Source: PubMed
Publication date: 2026/05/23
Franco GiovanniPromi SamueleGalbardi IsabellaPaciocco GiuseppeAllegranza PietroCangiotti CeciliaBono FrancescaZanini UmbertoPagni FabioFaverio PaolaGuerra LucaCortinovis Diego LuigiCazzaniga Marina ElenaLuppi Fabrizio - Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors are widely used in the treatment of estrogen receptor-positive (ER⁺) breast cancer; however, the metabolic adaptations induced by CDK4/6 inhibition remain incompletely defined. In ER⁺ breast cancer, estrogen signaling plays a central role in coordinating cell cycle progression and metabolic programs that support tumor growth. Glycolytic flux is regulated at the level of phosphofructokinase-1 (PFK1) through the inducible enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), which is transcriptionally regulated by estrogen receptor signaling and has been shown to promote glycolysis and proliferation in ER⁺ breast cancer cells. Yet, how CDK4/6 inhibition intersects with estrogen-regulated glycolytic control to rewire glucose utilization in ER⁺ breast cancer has not been explored. - Source: PubMed
Publication date: 2026/06/25
Telang SuchetaClem Brian FMiret Ariamna A HerreraPrice LeanneDougherty Susan MSchmitz AnnaYin XinminMa XipengZhang XiangChesney JasonImbert-Fernandez Yoannis