Description:

Size: 100ul

Catalog no.: bs-2969R-A594

Price: 380 EUR

Product details

Modification Site

None

Crossreactivity

Virus

Cross-reactive species details

HPV33

Subcellular location

Nucleus

Immunogen range

30-80/97

Target Antigen

HPV33 E7

Tested applications

IF(IHC-P)

French translation

anticorps

Modification

Unmodified

Clonality

Polyclonal

Excitation emission

590nm/617nm

Concentration

1ug per 1ul

Conjugated with

ALEXA FLUOR® 594

Conjugated

Alexa conjugate 1

Recommended dilutions

IF(IHC-P)(1:50-200)

Clone

Polyclonal antibody

Purification

Purified by Protein A.

Category

Conjugated Primary Antibodies

Conjugation

Alexa Fluor,ALEXA FLUOR® 594

Host Organism

Rabbit (Oryctolagus cuniculus)

Also known as

Anti-HPV33 E7 PAb ALEXA FLUOR 594

Specificity

This is a highly specific antibody against HPV33 E7.

Source

KLH conjugated synthetic peptide derived from HPV33 E7

Long name

HPV33 E7 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated

Storage conditions

Store this antibody in aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Keep refrigerated at 2 to 8 degrees Celcius for up to one year.

Synonyms

E7 protein [Human papillomavirus type 33]; Human Papilloma Virus; Human papillomavirus type 33; Human papillomavirus type 33; Protein 33; early protein E7 [Human papillomavirus type 33].

Properties

For facs or microscopy Alexa 1 conjugate.If you buy Antibodies supplied by Bioss Primary Conjugated Antibodies. ALEXA FLUOR they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

Background of the antigen

E7 protein has both transforming and trans-activating activities. Disrupts the function of host retinoblastoma protein RB1/pRb, which is a key regulator of the cell cycle. Induces the disassembly of the E2F1 transcription factors from RB1, with subsequent transcriptional activation of E2F1-regulated S-phase genes. Inactivation of the ability of RB1 to arrest the cell cycle is critical for cellular transformation, uncontrolled cellular growth and proliferation induced by viral infection. Stimulation of progression from G1 to S phase allows the virus to efficiently use the cellular DNA replicating machinery to achieve viral genome replication. Interferes with histone deacetylation mediated by HDAC1 and HDAC2, leading to activation of transcription (By similarity).