Description:

Size: 100ul

Catalog no.: bs-1252R-A594

Price: 380 EUR

Product details

Gene ID Number

8539

Target Antigen

API5

Modification Site

None

Swiss Prot

Q9BZZ5

Tested applications

IF(IHC-P)

French translation

anticorps

Modification

Unmodified

Clonality

Polyclonal

Concentration

1ug per 1ul

Excitation emission

590nm/617nm

Immunogen range

345-395/524

Conjugated

Alexa conjugate 1

Conjugated with

ALEXA FLUOR® 594

Crossreactivity

Human, Mouse, Rat

Subcellular location

Cytoplasm, Nucleus

Recommended dilutions

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

Clone

Polyclonal antibody

Purification

Purified by Protein A.

Conjugation

Alexa Fluor,ALEXA FLUOR® 594

Category

Conjugated Primary Antibodies

Also known as

Anti-API5 PAb ALEXA FLUOR 594

Host Organism

Rabbit (Oryctolagus cuniculus)

Specificity

This is a highly specific antibody against API5.

Long name

API5 Polyclonal Antibody, ALEXA FLUOR 594 Conjugated

Cross-reactive species details

Due to limited amount of testing and knowledge, not every possible cross-reactivity is known.

Source

This antibody was obtained by immunization of the host with KLH conjugated synthetic peptide derived from human API5

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

AAC11; AAC-11; Apoptosis inhibitor 5; API-5; Antiapoptosis clone 11 protein; Cell migration-inducing gene 8 protein; Fibroblast growth factor 2-interacting factor; FIF; Protein XAGL; API5; MIG8

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

Antiapoptotic factor that may have a role in protein assembly. Negatively regulates ACIN1. By binding to ACIN1, it suppresses ACIN1 cleavage from CASP3 and ACIN1-mediated DNA fragmentation. Also known to efficiently suppress E2F1-induced apoptosis. Its depletion enhances the cytotoxic action of the chemotherapeutic drugs.