Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

HMBS Mouse anti-Human, Clone: OTI1F1, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA526541

Catalog No. PIMA526541


Add to cart

Description

Description

PBGD (porphobilinogen deaminase), also designated hydroxymethylbilane synthase, is a cytoplasmic enzyme found in the heme synthesis pathway. PBGD belongs to the HMBS (hydroxymethylbilane synthase) family. Deficiency of PBGD causes errors in pyrrole metabolism, which in turn leads to an inherited autosomal disorder called acute intermittent porphyria (AIP). AIP is characterized by acute attacks of neurological dysfunctions with hypertension, tachycardia, peripheral neurologic disturbances, abdominal pain and excessive amounts of aminolevulinic acid and porphobilinogen in the urine.
Specifications

Specifications

HMBS
Monoclonal
1 mg/mL
PBS with 1% BSA, 50% glycerol and 0.02% sodium azide; pH 7.3
P08397
HEM3, HMBS, Hydroxymethylbilane synthase, PBG D, PBG-D, PBGD, Porphobilinogen deaminase, Pre uroporphyrinogen synthase, Pre-uroporphyrinogen synthase, UPS, Uroporphyrinogen I synthase, Uroporphyrinogen I synthetase
Mouse
IgG1
100 μL
-20° C, Avoid Freeze/Thaw Cycles
Primary
3145
Western Blot
OTI1F1
Unconjugated
HMBS
Liquid
HMBS
Full length human recombit protein of HMBS produced in HEK293T cell
Affinity Chromatography
RUO
Antibody
Monoclonal
Human
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit