Thermo Fisher Scientific LYNX1 Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1.0 µg/mL

-

Product Specifications

Species Reactivity

Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

synthetic peptide directed towards the middle region of human LYNX1

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

0.5 mg/mL

Purification

Affinity chromatography

Storage buffer

PBS with 2% sucrose

Contains

0.09% sodium azide

Storage conditions

-20° C, Avoid Freeze/Thaw Cycles

Shipping conditions

Wet ice

RRID

AB_2690510

Product Specific Information

This target displays homology in the following species: Cow: 100%; Guinea Pig: 100%; Human: 100%; Mouse: 93%; Rat: 93%

Target Information

LYNX1 acts in different tissues through interaction to nicotinic acetylcholine receptors (nAChRs). The proposed role as modulator of nAChR activity seems to be dependent on the nAChR subtype and stoichiometry, and to involve an effect on nAChR trafficking and its cell surface expression, and on single channel properties of the nAChR inserted in the plasma membrane. Modulates functional properties of nicotinic acetylcholine receptors (nAChRs) to prevent excessive excitation, and hence neurodegeneration. Enhances desensitization by increasing both the rate and extent of desensitization of alpha-4:beta-2-containing nAChRs and slowing recovery from desensitization. Promotes large amplitude ACh-evoked currents through alpha-4:beta-2 nAChRs. Is involved in regulation of the nAChR pentameric assembly in the endoplasmic reticulum. Shifts stoichiometry from high sensitivity alpha-4(2):beta-2(3) to low sensitivity alpha-4(3):beta-2(2) nAChR. In vitro modulates alpha-3:beta-4-containing nAChRs. Reduces cell surface expression of (alpha-3:beta-4)(2):beta-4 and (alpha-3:beta-4)(2):alpha-5 nAChRs suggesting an interaction with nAChR alpha-3(-):(+)beta-4 subunit interfaces and an allosteric mode. Corresponding single channel effects characterized by decreased unitary conductance, altered burst proportions and enhanced desensitization/inactivation seem to depend on nAChR alpha:alpha subunit interfaces and are greater in (alpha-3:beta-2)(2):alpha-3 when compared to (alpha-3:beta-2)(2):alpha-5 nAChRs. Prevents plasticity in the primary visual cortex late in life.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.