CDC2 ELISA Kit (DEIA-XYA370)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cultured cells
Species Reactivity
Human, Mouse, Rat
Intended Use
The CDC2 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor CDC2 protein expression profile in cells. The kit can be used for measuring the relative amounts of CDC2 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on CDC2.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 1 plate
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-CDC2 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


Targeting Wnt/EZH2/microRNA-708 signaling pathway inhibits neuroendocrine differentiation in prostate cancer

CELL DEATH DISCOVERY

Authors: Shan, Jingxuan; Al-Muftah, Mariam A.; Al-Kowari, Moza K.; Abuaqel, Sirin W. J.; Al-Rumaihi, Khalid; Al-Bozom, Issam; Li, Pu; Chouchane, Lotfi

Prostate cancer (PC) castration resistance has been linked to the differentiation of PC luminal cells into hormone-refractory neuroendocrine (NE) cells. However, the molecular mechanisms controlling the emergence of lethal NE prostate cancer (NEPC) remain unclear. The present study aimed to investigate the mechanisms underlying the transition from prostate adenocarcinoma to NEPC. The microRNA miR-708 was involved in NE differentiation and was downregulated in NEPC cells and tumor specimens. miR-708 targeted Sestrin-3 to inhibit Forkhead Box O1 (FOXO1) phosphorylation, resulting in apoptosis of prostate adenocarcinoma cells and AKT-inactivated NEPC cells, the latter of which was consistent with the progression of tumor xenografts in mice under miR-708 treatment. In silico analysis of PC and NEPC tumor specimens suggested that the polycomb repressive complex subunit Enhancer of zeste homolog 2 (EZH2) was particularly overexpressed in NEPC. Notably, EZH2 bound to the miR-708 promoter and induced its silencing in NEPC. Inhibition of EZH2 prevented NE differentiation of PC cells. EZH2 expression was regulated by both Cyclin Dependent Kinase 1 (CDK1) and Wnt signaling. Silencing transcription factor 4 (TCF4), as a key protein in Wnt signaling, prevented NEPC formation. These results provide a molecular basis for the roles of miR-708 and EZH2 in NE differentiation in PC and highlight a new paradigm in NEPC formation and survival.

Phosphorylation of the histone demethylase KDM5B and regulation of the phenotype of triple negative breast cancer

SCIENTIFIC REPORTS

Authors: Yeh, I-Ju; Esakov, Emily; Lathia, Justin D.; Miyagi, Masaru; Reizes, Ofer; Montano, Monica M.

Epigenetic modifications are known to play critical roles in the expression of genes related to differentiation and dedifferentiation. Histone lysine demethylase KDM5B (PLU-1) catalyzes the demethylation of histone H3 on Lys 4 (H3K4), which results in the repression of gene expression. KDM5B is involved in regulation of luminal and basal cell specific gene expression in breast cancers. However, the mechanisms by which KDM5B is regulated in breast cancer, in particular in response to post-translational signals is not well-defined. Here, we demonstrate that KDM5B is phosphorylated at Ser1456 by the cyclin-dependent kinase 1 (CDK1). Phosphorylation of KDM5B at Ser1456 attenuated the occupancy of KDM5B on the promoters of pluripotency genes. Moreover, KDM5B inhibited the expression of pluripotency genes, SOX2 and NANOG, and decreased the stem cell population in triple-negative breast cancer cell lines (TNBC). We previously reported that the tumor suppressor HEXIM1 is a mediator of KDM5B recruitment to its target genes, and HEXIM1 is required for the inhibition of nuclear hormone receptor activity by KDM5B. Similarly, HEXIM1 is required for regulation of pluripotency genes by KDM5B.

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