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Providers / Bioss Primary Conjugated Antibodies. ALEXA FLUOR / DDAH1 Antibody, ALEXA FLUOR 594

Description:

Size: 100ul

Catalog no.: bs-11997R-A594

Price: 380 EUR

Get for 380 EUR on Gentaur.com

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Product details

Modification Site

None

Target Antigen

DDAH1

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-DDAH1 PAb ALEXA FLUOR 594

Specificity

This is a highly specific antibody against DDAH1.

Long name

DDAH1 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 DDAH1

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.

Synonyms

DDAH; DDAH I; DDAH-1; DDAH1; DDAH1_HUMAN; DDAHI; Dimethylargininase 1; Dimethylargininase-1; Dimethylarginine dimethylaminohydrolase 1; NG; NG-dimethylarginine dimethylaminohydrolase 1; NG NG dimethylarginine dimethylaminohydrolase.

Background of the antigen

DDAH, a dimethylarginine dimethylaminohydrolase, hydrolyzes dimethyl arginine (ADMA) and monomethyl arginine (MMA), both inhibitors of nitric oxide synthases, and may be involved in in-vivo modulation of nitric oxide production (1,2). Impairment of DDAH causes ADMA accumulation and a reduction in cGMP generation (3). DDAH II, the predominant DDAH isoform in endothelial cells, facilitates the induction of nitric oxide synthesis by all-trans-Retinoic acid (atRA) (4). DDAH proteins are highly expressed in colon, kidney, stomach and liver tissues (1).