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Salubrinal

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This is an old revision of this page, as edited by CheMoBot (talk | contribs) at 20:48, 20 September 2011 (Updating {{drugbox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report [[Misplaced Pages talk:WikiProj). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Revision as of 20:48, 20 September 2011 by CheMoBot (talk | contribs) (Updating {{drugbox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report [[Misplaced Pages talk:WikiProj)(diff) ← Previous revision | Latest revision (diff) | Newer revision → (diff) Pharmaceutical compound
Salubrinal
Identifiers
IUPAC name
  • 3-phenyl-N-[2,2,2-trichloro-1-[[(8-quinolinylamino)thioxomethyl]amino]ethyl]-2-propenamide
CAS Number
CompTox Dashboard (EPA)
ECHA InfoCard100.237.268 Edit this at Wikidata
Chemical and physical data
FormulaC21H17Cl3N4OS
Molar mass479.81  g·mol
  (verify)

Salubrinal is a drug which acts as a specific inhibitor of eIF2α phosphatase enzymes and is primarily used experimentally, to study stress responses in eukaryotic cells associated with the action of eIF2. Salbrinal indirectly inhibits eIF2 as a result of reduced dephosphorylation of its α-subunit, resulting in activation of stress response pathways usually triggered by events such as oxidative stress or buildup of unfolded protein in the endoplasmic reticulum. Salubrinal has putative therapeutic value due to its function, but is as yet only used experimentally. Salubrinal is being studied at Indiana University for its potential to fight osteoporosis and accelerate bone healing.

References

  1. "SALUBRINAL | 405060-95-9". ChemicalBook. Retrieved 2010-10-05.
  2. "Salubrinal: sc-202332" (PDF). Santa Cruz Biotechnology, Inc. 2010-07-28. Retrieved 2010-10-05.
  3. ^ Lewerenz, Jan; Maher, Pamela (2009-01-09). "Basal Levels of eIF2α Phosphorylation Determine Cellular Antioxidant Status by Regulating ATF4 and xCT Expression". The Journal of Biological Chemistry. 284 (2). The American Society for Biochemistry and Molecular Biology, Inc: 1106. doi:10.1074/jbc.M807325200.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. Kessel, David (2006-08-11). "Protection of Bcl-2 by sulubrinal". Biochemical and Biophysical Research Communications. 346 (4). Elsevier Inc: 1320. doi:10.1016/j.bbrc.2006.06.056. PMID 16806073. Retrieved 2010-10-05.
  5. ^ Boyce M, Bryant KF, Jousse C, Long K, Harding HP, Scheuner D, Kaufman RJ, Ma D, Coen DM, Ron D, Yuan J (2005). "A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress". Science. 307 (5711): 935–9. doi:10.1126/science.1101902. PMID 15705855. Retrieved 2010-10-05. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. "Entrez Gene: EIF2S1 eukaryotic translation initiation factor 2, subunit 1 alpha, 35kDa". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 2010-10-05.
  7. "Coping with stress: eIF2 kinases and translational control" (PDF). Biochemical Society Transactions. 34 (1). Biochemical Society: 7–11. 2006. PMID 16246168. Retrieved 2010-10-05. {{cite journal}}: Unknown parameter |authors= ignored (help); Unknown parameter |month= ignored (help)
  8. "New compound may accelerate bone healing, prevent osteoporosis". 2011. Retrieved 2011-29-08. {{cite web}}: Check date values in: |accessdate= (help); Unknown parameter |month= ignored (help)


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