Description:

Size: 100ul

Catalog no.: bs-11470R-A555

Price: 380 EUR

Product details

Modification Site

None

Gene ID Number

5365

Swiss Prot

Q9ULL4

French translation

anticorps

Target Antigen

Plexin B3

Tested applications

IF(IHC-P)

Modification

Unmodified

Clonality

Polyclonal

Excitation emission

553nm/568nm

Concentration

1ug per 1ul

Immunogen range

360-400/1909

Subcellular location

Extracellular

Crossreactivity

Human, Mouse, Rat

Conjugated with

ALEXA FLUOR® 555

Recommended dilutions

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

Clone

Polyclonal antibody

Purification

Purified by Protein A.

Conjugation

Alexa Fluor,ALEXA FLUOR 555

Category

Conjugated Primary Antibodies

Host Organism

Rabbit (Oryctolagus cuniculus)

Also known as

Anti-Plexin B3 PAb ALEXA FLUOR 555

Synonyms

PLEXR; PLXN6; PLEXB3; Plexin-B3; PLXNB3; KIAA1206

Specificity

This is a highly specific antibody against Plexin B3.

Long name

Plexin B3 Polyclonal Antibody, ALEXA FLUOR 555 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 Plexin B2

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.

Properties

For facs or microscopy Alexa 1 conjugate.Very high photo stable ALEXA 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

Receptor for SEMA5A that plays a role in axon guidance, invasive growth and cell migration. Stimulates neurite outgrowth and mediates Ca(2+)/Mg(2+)-dependent cell aggregation. In glioma cells, SEMA5A stimulation of PLXNB3 results in the disassembly of F-actin stress fibers, disruption of focal adhesions and cellular collapse as well as inhibition of cell migration and invasion through ARHGDIA-mediated inactivation of RAC1.