Cyclin A2 Antibody [N5C11] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IP1:100 IHC1:800 - 1:3200 IF1:400 - 1:1600 FCM1:400 - 1:1600

Application
WB, IP, IHC, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
55 kDa

Positive Control	Human colon carcinoma; Human urothelial carcinoma; Human thymus; Human non-small cell lung carcinoma; Human large cell neuroendocrine carcinoma; Human small cell carcinoma of the salivary gland; HT-29 cells (Aphidicolin, 10 µg/ml, 24 h); HCT 116 cells; A549 cells; K-562 cells
Negative Control	CaKi-1 cells

Datasheet & SDS

Biological Description

Specificity
Cyclin A2 Antibody [N5C11] detects endogenous levels of total Cyclin A2 protein.

Clone
N5C11

Synonym(s)
Cyclin-A2; Cyclin-A; Cyclin A; CCNA2; CCN1; CCNA

Background
Cyclin A2 (CCNA2), a key member of the cyclin family, orchestrates S-phase progression and the G2/M transition by sequentially binding and activating CDK2 during S-phase and CDK1 at the onset of mitosis, with its levels peaking from late G1 through prometaphase before being targeted for ubiquitin-mediated degradation. Cyclin A2 features an N-terminal extension with a flexible α-helix critical for CDK docking and RhoA binding, two cyclin box folds composed of α1–5 helices that form a hydrophobic interface for CDK interaction, and a C-terminal domain containing a poorly conserved RNA-binding region that interacts with Mre11 mRNA. Mutagenesis studies highlight the importance of the α3 helix and N-terminal motif for both CDK activation and nuclear localization. Cyclin A2 integrates CDK-dependent phosphorylation of replication factors such as Treslin for origin firing and Cdc6 for licensing to drive DNA synthesis, and phosphorylates T926 on Eg5 to facilitate centrosomal loading and spindle bipolarity. Cyclin A2 binds the 3'UTR of Mre11 mRNA and interacts with eIF4A2 to enhance translation of homologous recombination repair proteins like MRE11 and RAD51, thereby stabilizing DNA repair. Its N-terminus also potentiates RhoA-GEF activity, which suppresses cell invasion by stabilizing cortical F-actin. Cyclin A2 ensures timely progression through S and M phases, maintains replication fidelity, supports double-strand break repair, and restrains cell motility. Loss of Cyclin A2 leads to chromosomal instability, replication stress, and tumorigenesis in mouse models, while its overexpression is associated with poor prognosis in breast and gynecologic cancers due to increased genomic instability.

Background

Cyclin A2 (CCNA2), a key member of the cyclin family, orchestrates S-phase progression and the G2/M transition by sequentially binding and activating CDK2 during S-phase and CDK1 at the onset of mitosis, with its levels peaking from late G1 through prometaphase before being targeted for ubiquitin-mediated degradation. Cyclin A2 features an N-terminal extension with a flexible α-helix critical for CDK docking and RhoA binding, two cyclin box folds composed of α1–5 helices that form a hydrophobic interface for CDK interaction, and a C-terminal domain containing a poorly conserved RNA-binding region that interacts with Mre11 mRNA. Mutagenesis studies highlight the importance of the α3 helix and N-terminal motif for both CDK activation and nuclear localization. Cyclin A2 integrates CDK-dependent phosphorylation of replication factors such as Treslin for origin firing and Cdc6 for licensing to drive DNA synthesis, and phosphorylates T926 on Eg5 to facilitate centrosomal loading and spindle bipolarity. Cyclin A2 binds the 3'UTR of Mre11 mRNA and interacts with eIF4A2 to enhance translation of homologous recombination repair proteins like MRE11 and RAD51, thereby stabilizing DNA repair. Its N-terminus also potentiates RhoA-GEF activity, which suppresses cell invasion by stabilizing cortical F-actin. Cyclin A2 ensures timely progression through S and M phases, maintains replication fidelity, supports double-strand break repair, and restrains cell motility. Loss of Cyclin A2 leads to chromosomal instability, replication stress, and tumorigenesis in mouse models, while its overexpression is associated with poor prognosis in breast and gynecologic cancers due to increased genomic instability.

References
https://pubmed.ncbi.nlm.nih.gov/26629317/ https://pubmed.ncbi.nlm.nih.gov/27708105/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%