Description:

Size: 100ul

Catalog no.: bs-11717R-A594

Price: 380 EUR

Product details

Modification Site

None

Target Antigen

CTRP5

French translation

anticorps

Tested applications

IF(IHC-P)

Clonality

Polyclonal

Modification

Unmodified

Concentration

1ug per 1ul

Excitation emission

590nm/617nm

Conjugated with

ALEXA FLUOR® 594

Crossreactivity

Human, Mouse, Rat

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-CTRP5 PAb ALEXA FLUOR 594

Specificity

This is a highly specific antibody against CTRP5.

Long name

CTRP5 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 CTRP5

Synonyms

C1q and tumor necrosis factor related protein 5; C1QTNF5; Complement C1q tumor necrosis factor related protein 5 precursor; LORD; C1QT5_HUMAN.

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.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

Members of the C1q superfamily have diverse functions that are related to cell adhesion and basement membrane components. CTRP5 (Complement C1q tumor necrosis factor-related protein 5) is a 243 amino acid secreted and membrane-associated protein that contains a collagen-like domain and a C1q domain. CTRP5 is a short-chain collagen that is expressed in retinal pigment epithelium as well as brain, lung, liver and placenta. By forming an extracellular hexagonal lattice, CTRP5 facilitates the adhesion of basal retinal pigment epithelium to Bruch’s membrane, the innermost layer of the choroid. A mutation within the C1q domain of CTRP5 results in abnormal high molecular weight aggregate formation, which alters its structure and interactions. This mutation may result in the presentation of late-onset retinal degeneration (LORD), an autosomal dominant disorder that is characterized by punctate yellow-white deposits in the retinal fundus and night blindness.