ALEXIS Biochemicals: Polyclonal Antibody to α-Epithelial Cell Sodium Channel (rat)

ALX-210-291

Revised 16-Feb-05

Polyclonal Antibody to α-Epithelial Cell Sodium Channel (rat)
SYNONYMS	anti-α-ENaC (rat) PAb
PRODUCT LINE	Signal Transduction
PRODUCT CATEGORY	Na+ Channels

Ordering Information

Product Numbers:	Format:	Size:	Unit Price:	Quantity:	Add To Cart
ALX-210-291-C100		100 µg	379.00 USD

Product Specification

SPECIES CROSSREACTIVITY:	Rat
SOURCE/HOST:	From rabbit.
CONCENTRATION:	1mg/ml.
FORMULATION:	Liquid. Epitope-affinity purified IgG in PBS containing 1mg/ml BSA and 0.05% sodium azide.
IMMUNOGEN:	Synthetic peptide corresponding to aa 20-42 (L²⁰MKGNKREEQGL GPEPAAPQQPT⁴²C) of human ENACα (epithelial cell sodium channel α).
SPECIFICITY:	Recognizes rat α-ENaC. Detects a band of ~97kDa (glycosylated form) by Western blot. Specifically binds to unglycosylated ~75kDa α-ENaC by IP.
APPLICATION:	Immunoprecipitation Western Blot (1µg/ml)
SHIPPING:	SHIPPED ON BLUE ICE
LONG TERM STORAGE:	-20°C
HANDLING:	Avoid freeze/thaw cycles.
BLOCKING PEPTIDE:	For Blocking Peptide see Prod. No. ALX-155-035.

Product Description

Epithelial sodium channels are amiloride-sensitive members of the degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this superfamily of ion channels share organizational similarity in that they all possess two short intracellular amino and carboxyl termini, two short membrane-spanning segments, and a large extracellular loop domain with a conserved cysteine-rich region. There are 3 homologous isoforms of the EnaC (α, β and γ) protein. ENaC in the kidney, lung, and colon plays an essential role in transepithelial Na⁺ and fluid balance. ENaC also mediates aldosterone-dependent (Prod.No. 804-099) sodium reabsorption in the distal nephron of the kidney, thus regulating blood pressure. ENaC is thought to be regulated, in part, through association with the cystic fibrosis transmembrane conductance regulator (Prod.No. 804-214) chloride ion channel. Gain-of-function mutations in β- or γ-ENaC can cause severe arterial hypertension (Liddle's syndrome) and loss-of-function mutations in α- or β-ENaC pseudohypoaldosteronism (PHA-1).

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Polyclonal Antibodies

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