Cyclin A1 + A2 Antibody (Rabbit mAb) [N12H18]

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IP1:70 IHC1:2000

Application
WB, IP, IHC

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 Observed MW
52 kDa 52 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
Cyclin A1 + A2 Antibody (Rabbit mAb) [N12H18] detects endogenous levels of total Cyclin A1 and A2 protein.

Clone
N12H18

Synonym(s)
Cyclin-A1, CCNA1, CCN1, CCNA, CCNA2, Cyclin-A2, Cyclin-A, Cyclin A

Background
Cyclin A1 and cyclin A2 are A‑type cyclins that form regulatory subunits of cyclin‑dependent kinases and together coordinate key transitions of the germline meiotic and somatic mitotic cell cycles, with cyclin A1 showing restricted expression in male germ cells and cyclin A2 displaying broad expression in proliferating somatic tissues. Both proteins share the characteristic cyclin box fold that provides the interface for binding CDKs, but they differ in expression timing and partner usage: cyclin A1 binds Cdk2 and Cdk1 in late pachytene and diplotene spermatocytes and is present around the first meiotic division, whereas cyclin A2 is abundant in spermatogonia and preleptotene spermatocytes and associates primarily with Cdk2 in germ cells, reflecting distinct functions in meiotic entry versus passage through meiosis. During male meiosis, cyclin A1 is required for progression from G2 into metaphase I; targeted disruption of the Ccna1 gene causes spermatogenic arrest before metaphase I, with defective activation of Cdc2 kinase and failure to generate active M‑phase‑promoting factor despite retention of B‑type cyclins, and cyclin A1–Cdc2/Cdk2 complexes can phosphorylate Cdc25A and Cdc25C phosphatases, indicating that cyclin A1 participates in an amplification loop that drives MPF activation and the G2/M transition in spermatocytes. Immunolocalization studies in testis show that cyclin A1 protein appears in germ cells just prior to or during the first meiotic division and then disappears, while cyclin A2 is expressed earlier in spermatogonia and preleptotene spermatocytes entering the meiotic pathway, and cyclin A1‑dependent kinase activity toward histone H1 is detectable in germ‑cell lysates, supporting a role for cyclin A1‑CDK complexes in chromatin condensation and meiotic chromosome segregation. In contrast, cyclin A2 is synthesized at the onset of S phase in somatic cells and binds Cdk2 to initiate and maintain DNA replication and prevent re‑replication by phosphorylating licensing factors such as CDC6 and MCM proteins, then later binds Cdk1 to promote G2/M progression and trigger activation of cyclin B1–Cdk1 complexes that drive chromatin condensation and nuclear envelope breakdown, making cyclin A2 a central regulator of both G1/S and G2/M transitions in the mitotic cycle. During mouse development and early embryogenesis, cyclin A2 is ubiquitously expressed in dividing cells and controls both DNA replication and spindle assembly, while cyclin A1 expression is restricted to spermatocytes, leukemia cells and certain post‑mitotic multiciliated cells, indicating that their differential expression patterns and CDK partner usage underpin specialization of A‑type cyclin function in germline versus somatic cell cycles. Genetic and functional work shows that cyclin A1 is essential for male fertility, with cyclin A1 haplo‑insufficiency reducing sperm count and quality, whereas cyclin A2 knockout is embryonic lethal due to failure of mitotic proliferation, underscoring that cyclin A1 is a critical meiotic regulator while cyclin A2 is indispensable for general cell division. Both cyclin A1 and A2 are implicated in tumor biology: cyclin A2 is frequently overexpressed in diverse cancers, where its elevated levels correlate with poor prognosis and may contribute to genomic instability through altered S‑phase and G2/M control, and cyclin A1 is expressed in certain leukemias and solid tumors, reflecting dysregulated germline cell‑cycle regulators in malignant contexts. A‑type cyclins A1 and A2 constitute a structurally related pair of CDK partners whose distinct expression domains and kinase interactions orchestrate G1/S and G2/M transitions across meiosis and mitosis, with cyclin A1 driving MPF activation and first meiotic division in male germ cells and cyclin A2 governing S‑phase entry, DNA replication fidelity and mitotic onset in somatic lineages, making this cyclin pair an informative target set for studies of cell‑cycle control, gametogenesis and cancer.

Background

Cyclin A1 and cyclin A2 are A‑type cyclins that form regulatory subunits of cyclin‑dependent kinases and together coordinate key transitions of the germline meiotic and somatic mitotic cell cycles, with cyclin A1 showing restricted expression in male germ cells and cyclin A2 displaying broad expression in proliferating somatic tissues. Both proteins share the characteristic cyclin box fold that provides the interface for binding CDKs, but they differ in expression timing and partner usage: cyclin A1 binds Cdk2 and Cdk1 in late pachytene and diplotene spermatocytes and is present around the first meiotic division, whereas cyclin A2 is abundant in spermatogonia and preleptotene spermatocytes and associates primarily with Cdk2 in germ cells, reflecting distinct functions in meiotic entry versus passage through meiosis. During male meiosis, cyclin A1 is required for progression from G2 into metaphase I; targeted disruption of the Ccna1 gene causes spermatogenic arrest before metaphase I, with defective activation of Cdc2 kinase and failure to generate active M‑phase‑promoting factor despite retention of B‑type cyclins, and cyclin A1–Cdc2/Cdk2 complexes can phosphorylate Cdc25A and Cdc25C phosphatases, indicating that cyclin A1 participates in an amplification loop that drives MPF activation and the G2/M transition in spermatocytes. Immunolocalization studies in testis show that cyclin A1 protein appears in germ cells just prior to or during the first meiotic division and then disappears, while cyclin A2 is expressed earlier in spermatogonia and preleptotene spermatocytes entering the meiotic pathway, and cyclin A1‑dependent kinase activity toward histone H1 is detectable in germ‑cell lysates, supporting a role for cyclin A1‑CDK complexes in chromatin condensation and meiotic chromosome segregation. In contrast, cyclin A2 is synthesized at the onset of S phase in somatic cells and binds Cdk2 to initiate and maintain DNA replication and prevent re‑replication by phosphorylating licensing factors such as CDC6 and MCM proteins, then later binds Cdk1 to promote G2/M progression and trigger activation of cyclin B1–Cdk1 complexes that drive chromatin condensation and nuclear envelope breakdown, making cyclin A2 a central regulator of both G1/S and G2/M transitions in the mitotic cycle. During mouse development and early embryogenesis, cyclin A2 is ubiquitously expressed in dividing cells and controls both DNA replication and spindle assembly, while cyclin A1 expression is restricted to spermatocytes, leukemia cells and certain post‑mitotic multiciliated cells, indicating that their differential expression patterns and CDK partner usage underpin specialization of A‑type cyclin function in germline versus somatic cell cycles. Genetic and functional work shows that cyclin A1 is essential for male fertility, with cyclin A1 haplo‑insufficiency reducing sperm count and quality, whereas cyclin A2 knockout is embryonic lethal due to failure of mitotic proliferation, underscoring that cyclin A1 is a critical meiotic regulator while cyclin A2 is indispensable for general cell division. Both cyclin A1 and A2 are implicated in tumor biology: cyclin A2 is frequently overexpressed in diverse cancers, where its elevated levels correlate with poor prognosis and may contribute to genomic instability through altered S‑phase and G2/M control, and cyclin A1 is expressed in certain leukemias and solid tumors, reflecting dysregulated germline cell‑cycle regulators in malignant contexts. A‑type cyclins A1 and A2 constitute a structurally related pair of CDK partners whose distinct expression domains and kinase interactions orchestrate G1/S and G2/M transitions across meiosis and mitosis, with cyclin A1 driving MPF activation and first meiotic division in male germ cells and cyclin A2 governing S‑phase entry, DNA replication fidelity and mitotic onset in somatic lineages, making this cyclin pair an informative target set for studies of cell‑cycle control, gametogenesis and cancer.

References
https://pubmed.ncbi.nlm.nih.gov/21630154/ https://pubmed.ncbi.nlm.nih.gov/10068472/

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%