Recombinant Cyclin E1 antibody (AA 10-176)

Catalog No. ABIN7869685

The Rabbit Monoclonal anti-Cyclin E1 antibody (Clone CCNE1-4935R) (ABIN7869685) specifically detects Cyclin E1 in WB and IHC (p). The antibody is reactive with Human samples.

Quick Overview for Recombinant Cyclin E1 antibody (AA 10-176) (ABIN7869685)

Target: Cyclin E1 (CCNE1)

Antibody Type: Recombinant Antibody

Reactivity: Human

Host: Rabbit

Clonality: Monoclonal

Conjugate: This Cyclin E1 antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Grade: Carrier-free

Clone: CCNE1-4935R

Product Details anti-Cyclin E1 Antibody

Binding Specificity: AA 10-176

Purpose: Recombinant CCNE1 Antibody / Cyclin E1 (azide and preservative free)

Purification: Protein A/G affinity

Immunogen: A portion of amino acids 10-176 was used as the immunogen for the recombinant CCNE1 antibody.

Isotype: IgG

Application Details

Application Notes: Optimal dilution of the recombinant CCNE1 antibody should be determined by the researcher.

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 mg/mL

Buffer: 1 mg/mL in 1X PBS, BSA free, sodium azide free

Preservative: Azide free

Storage: -20 °C

Storage Comment: Aliquot the recombinant CCNE1 antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles.

Target Details for Cyclin E1

Target: Cyclin E1 (CCNE1)

Alternative Name: CCNE1

Background: Cyclin E belongs to the highly conserved cyclin family, whose members exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. Cyclins function as regulators of CDK kinases. Cyclin E forms a complex with and functions as a regulatory subunit of CDK2, whose activity is required for cell cycle G1/S transition. Cyclin E accumulates at the G1-S phase boundary and is degraded as cells progress through S phase. Cyclin E overexpression has been observed in many tumors, which results in chromosome instability, and thus may contribute to tumorigenesis.

Pathways: Cell Division Cycle, Intracellular Steroid Hormone Receptor Signaling Pathway, Nuclear Hormone Receptor Binding, Mitotic G1-G1/S Phases