U0126

U0126

Material name by the IUPAC glossology
IUPAC name 1,4-diamino-2,3-dicyano-1,4-bis (2-aminophenylthio)butadiene
Identification
CAS number (MeSH)	109,522-58-2
PubChem	CID: 5354033
ChEMBL	CHEMBL100473
Chemical data
Chemical formula	C18H16N6S2
Molecular weight	380.49 g/mol

U0126 is a high selective inhibitor of MEK1 (English version) which is a kind of the MAPK/ERK kinase and MEK2 (English version) [¹]. U0126 is IC₅0 72 nM in MEK1 which is double specific kinase, and it is found that I compete with AP-1 transcription activity functionally by inhibiting MEK2 noncompetitively in 58 nM [²].

U0126 is cell outside signal adjustment kinase (ERK) course and mammalian rapamycin target protein (mTOR) -I obstruct the rat fibroblastic anchorage independent increase that Ki-ras was transformed by interfering with p70(S6K) course at the same time. In the examination for the increase of eight kinds of breast cancer cell strain of the Homo sapiens, it is shown that U0126 controls the anchorage independent increase of MDA-M231 where ERK is activated constitutively and the HBC4 cell selectively [³]. When the contact with the substrate out of the cell is lost in much normalcy cells, apoptosis is caused (that stetting anoikis). U0126 does MDA-MB231 and HBC4 in sensitivity for that stetting. In other words, as for the cell, the cell which was robbed of its scaffold advances to the apoptosis when I handle U0126.

U0126 is protein kinase C (PKC), Raf, ERK, JNK, MEKK, MKK-3, MKK-4/SEK, MKK-6, Cdk2, a repressor having weak Cdk4 again.

In addition, it is known to cause slight memory loss, and there seems to be some evidence that this compound can use for treatment of the post-traumatic stress disorder (PTSD) [⁴].

Footnote

1. ^ Favata, M., et al. (1998). "Identification of a novel inhibitor of mitogen-activated protein kinase." J. Biol. Chem. 273: 18623-18632. doi: 10.1074/jbc.273.29.18623. 
2. ^ Duncia, J. V., et al.. "MEK inhibitors: The chemistry and biological activity of U0126, its analogs, and cyclization products." Bioorg. Med. Chem. Lett. 8: 2839-2844. doi: 10.1016/S0960-894X(98) 00522-8. PMID 9873633. 
3. ^ Fukazawa, H.; Noguchi, K.; Murakami, Y.; Uehara, Y. (2002). "Mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) inhibitors restore anoikis sensitivity in human breast cancer cell lines with a constitutively activated extracellular-regulated kinase (ERK) pathway". Mol. Cancer Ther. 1: 303-309. http://mct.aacrjournals.org/content/1/5/303.abstract. 
4. ^ Smith, Kerri (March 11, 2007). "Wipe out a single memory". Nature News. doi: 10.1038/news070305-17. June 20, 2012 reading.

References

• DeSilva DR, Jones EA, Favata MF, Jaffee BD, Magolda RL, Trzaskos JM, Scherle PA (1998). "Inhibition of mitogen-activated protein kinase blocks T cell proliferation but does not induce or prevent anergy." J. Immunol. It is 4175-4181 160. PMID 9574517. 

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