|Tested species reactivity||Human|
|Published species reactivity||Rat, Not Applicable|
|Host / Isotype||Mouse / IgG2b, kappa|
|Immunogen||Full-length recombinant human GRIM-19|
|Storage buffer||HEPES buffered saline|
|Contains||0.02% sodium azide|
|Storage Conditions||4° C, do not freeze|
|Tested Applications||Dilution *|
|Immunocytochemistry (ICC)||1.0 ug/ml|
|Immunofluorescence (IF)||Assay Dependent|
|Immunohistochemistry (IHC)||Assay Dependent|
|Western Blot (WB)||1.0 ug/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
A novel gene associated with Retinoid-IFN-induced Mortality (GRIM) GRIM-19 gene was identified. Antisense expression of GRIM-19 confers a strong resistance against IFN/RA-induced death by reducing the intracellular levels of GRIM-19 protein. Overexpression of GRIM-19 enhances cell death in response to IFN/RA. GRIM-19 is primarily a nuclear protein whose expression is induced by the IFN/RA combination. These data indicate that GRIM-19 is a novel cell death-regulatory molecule.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Rat||Not Cited||GDNF family ligand dependent STAT3 activation is mediated by specific alternatively spliced isoforms of GFR¿2 and RET.||Zhou L,Too HP||Biochimica et biophysica acta (1833:2789)||2013|
Mitochondrial localized STAT3 is involved in NGF induced neurite outgrowth.
43-8900 was used in immunocytochemistry to study the involvement of STAT3 phosphorylation in neurite outgrowth
|Zhou L,Too HP||PloS one (6:null)||2011|