E2F Transcription Factor 1 (E2F1) Antibody (Biotin)

Este producto es parte de E2F - E2F Transcription Factor
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169€ (20 µg)

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935106861
info@markelab.com
name
E2F Transcription Factor 1 (E2F1) Antibody (Biotin)
category
Primary Antibodies
provider
Abbexa
reference
abx312692
tested applications
ELISA

Description

E2F1 Antibody (Biotin) is a Rabbit Polyclonal against E2F1 conjugated to Biotin.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
E2F Transcription Factor 1 (E2F1)
Host
Rabbit
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Biotin
Isotype
IgG
Purity
> 95%
Purification
Purified by Protein G.
Size 1
20 µg
Size 2
50 µg
Size 3
100 µg
Size 4
200 µg
Size 5
1 mg
Form
Liquid
Tested Applications
ELISA
Buffer
0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q01094
Gene ID
1869
OMIM
189971
Alias
E2F-1,RBAP1,RBBP3,RBP3,Retinoblastoma-binding protein 3,Retinoblastoma-associated protein 1
Background
Antibody anti-E2F1
Status
RUO

Descripción

E2F1 is a member of the E2F family of transcription factors, which are critical regulators of cell cycle progression, DNA replication, and apoptosis. E2F1 drives the transition from G1 to S phase by activating genes required for DNA synthesis and cell proliferation, including cyclins and replication factors. It is tightly regulated by the retinoblastoma protein (pRB), which suppresses its activity under growth-inhibitory conditions. E2F1 also induces apoptosis under cellular stress or DNA damage by activating pro-apoptotic genes such as p53 and caspases. Dysregulation of E2F1 contributes to tumorigenesis by promoting uncontrolled proliferation and resistance to cell death. In cancer, overexpression of E2F1 is often observed, correlating with poor prognosis and enhanced tumor growth. Knockout models reveal defects in cell cycle progression and reduced apoptosis, emphasizing its dual role in proliferation and programmed cell death.

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