CCND2 peptide

Name: CCND2 peptide
SKU: DAG-P1490
Rating: 5 (1 reviews)

Synthetic CCND2 peptide

COA

SDS

Datasheet

Summary

Nature

Synthetic

Tag/Conjugate

Unconjugated

SequenceSimilarities

Belongs to the cyclin family. Cyclin D subfamily.Contains 1 cyclin N-terminal domain.

Purity

70 - 90% by HPLC.

Preservative

None

Storage

Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. Information available upon request.

Entrez Gene ID

894

Antigen Description

The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. This protein has been shown to interact with and be involved in the phosphorylation of tumor suppressor protein Rb. Knockout studies of the homologous gene in mouse suggest the essential roles of this gene in ovarian granulosa and germ cell proliferation. High level expression of this gene was observed in ovarian and testicular tumors. [provided by RefSeq, Oct 2008]

Function

protein binding; protein kinase binding;

Synonyms

CCND2; cyclin D2; KIAK0002; G1/S-specific cyclin-D2; G1/S-specific cyclin D2;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Methoxychlor inhibits growth of antral follicles by altering cell cycle regulators

TOXICOLOGY AND APPLIED PHARMACOLOGY

Authors: Gupta, Rupesh K.; Meachum, Sharon; Hernandez-Ochoa, Isabel; Peretz, Jackye; Yao, Humphrey H.; Flaws, Jodi A.

Abstract

Methoxychlor (MXC) reduces fertility in female rodents. decreases antral follicle numbers, and increases atresia through oxidative stress pathways. MXC also inhibits antral follicle growth in vitro. The mechanism by which MXC inhibits growth of follicles is unknown. The growth of follicles is controlled, in part, by cell cycle regulators. Thus, we tested the hypothesis that MXC inhibits follicle growth by reducing the levels of selected cell cycle regulators. Further, we tested whether co-treatment with an antioxidant, N-acetyl cysteine (NAC), prevents the MXC-induced reduction in cell cycle regulators. For in vivo studies, adult cycling CD-1 mice were dosed with MXC or vehicle for 20 days. Treated ovaries were subjected to immunohistochemistry for proliferating cell nuclear antigen (PCNA) staining. For in vitro studies, antral follicles isolated from adult cycling CD-1 mouse ovaries were Cultured with vehicle, MXC, and/or NAC for 48, 72 and 96 h. Levels of cyclin D2 (Ccnd2) and cyclin dependent kinase 4 (Cdk4) were measured using in vivo and in vitro samples. The results indicate that MXC decreased PCNA staining, and Ccnd2 and Cdk4 levels compared to controls. NAC co-treatment restored follicle growth and expression of Ccnd2 and Cdk4. Collectively, these data indicate that MXC exposure reduces the levels of Ccnd2 and Cdk4 in follicles, and that protection from oxidative stress restores Ccnd2 and Cdk4 levels. Therefore, MXC-induced oxidative Stress may decrease the levels of cell cycle regulators, which in turn, results in inhibition of the growth of antral follicles. (C) 2009 Elsevier Inc. All rights reserved.

miR-145 suppresses ovarian cancer progression via modulation of cell growth and invasion by targeting CCND2 and E2F3

MOLECULAR MEDICINE REPORTS

Authors: Hua, Minhui; Qin, Yongwei; Sheng, Meihong; Cui, Xiaopeng; Chen, Weiguan; Zhong, Jianxin; Yan, Junming; Chen, Yan

Abstract

MicroRNAs (miRNA/miRs) have been demonstrated to be critical post-transcriptional modulators of gene expression during tumorigenesis. Numerous miRNAs have been revealed to be downregulated in human epithelial ovarian cancer (EOC). In the present study, it was observed that the expression of miR-145 was decreased in EOC tissues and cell lines. Overexpression of miR-145 inhibited the proliferation, migration and invasion of EOC cells. The D-type cyclin 2, cyclin D2 (CCND2), and E2F transcription factor 3 (E2F3) were confirmed to be targets of miR-145. In addition, restoration of these 2 genes significantly reversed the tumor suppressive effects of miR-145. Collectively, the results indicated that miR-145 serves a critical role in suppressing the biological behavior of EOC cells by targeting CCND2 and E2F3. Therefore, miR-145 was suggested to be a potential miRNA-based therapeutic target in ovarian cancer.