- Featured Product
- KD/KO Validated
GSNOR,ADH5 Monoclonal antibody
GSNOR,ADH5 Monoclonal Antibody for IF, IHC, WB,ELISA
Cat no : 66193-1-Ig
|Positive WB detected in||HuH-7 cells, human testis tissue, HepG2 cells, fetal human brain tissue, pig liver tissue, rat brain tissue, rat liver tissue|
|Positive IHC detected in||human pancreas cancer tissue, human testis tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in||HepG2 cells|
|Western Blot (WB)||WB : 1:5000-1:50000|
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
66193-1-Ig targets GSNOR,ADH5 in WB, IHC, IF,ELISA applications and shows reactivity with human, mouse, rat, pig samples.
|Tested Reactivity||human, mouse, rat, pig|
|Host / Isotype||Mouse / IgG1|
|Immunogen||GSNOR,ADH5 fusion protein Ag9511|
|Full Name||alcohol dehydrogenase 5 (class III), chi polypeptide|
|Calculated molecular weight||374 aa, 40 kDa|
|Observed molecular weight||40 kDa|
|GenBank accession number||BC014665|
|Gene ID (NCBI)||128|
|Purification Method||Protein A purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
ADH5, also named as ADHX, FDH FALDH GSH-FDH ADH3 and GSNOR, belongs to the zinc-containing alcohol dehydrogenase family and Class-III subfamily. It is remarkably ineffective in oxidizing ethanol, but it readily catalyzes the oxidation of long-chain primary alcohols and the oxidation of S-(hydroxymethyl) glutathione. ADH5 mediates multiple cardiovascular functions. It plays in regulating heterocellular communication in the artery wall. (PMID:21071693). ADH5 immunostaining is distributed in both the nucleus and cytoplasm of the retinal ganglion cells(PMID:22117533).
Alzheimers Dement (N Y)
New insight into Alzheimer's disease: Light reverses Aβ-obstructed interstitial fluid flow and ameliorates memory decline in APP/PS1 mice.
Degradation of FA reduces Aβ neurotoxicity and Alzheimer-related phenotypes.