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SELE — SELL

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: SELE — SELL (physical association, affinity chromatography technology) Zöllner et al., J Cell Biol 1997*
• IRef Hprd Interaction: SELE — SELL (in vitro) Zöllner et al., J Cell Biol 1997*
• IRef Innatedb Interaction: SELL — SELE (unknown, -) Zöllner et al., J Cell Biol 1997*
• IRef Ophid Interaction: SELL — SELE (aggregation, confirmational text mining) Zöllner et al., J Cell Biol 1997*
• IRef Ophid Interaction: SELL — SELE (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Takei et al., Am J Hum Genet 2002 (Genetic Predisposition to Disease...) : SELE8 and SELL10 caused amino acid substitutions from His to Tyr and from Pro to Ser ( chi2=9.02, P=.0026, odds ratio = 2.73 [ 95 % confidence interval [ CI ] 1.38 -- 5.38 ] for His-to-Tyr substitutions ; chi2=17.4, P=.000031, odds ratio = 3.61 [ 95 % CI 1.91 -- 6.83 ] for Pro-to-Ser substitutions ), and SELL1 could affect promoter activity of the L-selectin gene ( chi2=19.5, P=.000010, odds ratio = 3.77 [ 95 % CI 2.02 -- 7.05 ] )
Yoshizaki et al., J Immunol 2010 (Fibrosis...) : This study suggests that L-selectin and ICAM-1 regulate Th2 and Th17 cell accumulation into the skin and lung, leading to the development of fibrosis, and that P-selectin, E-selectin , and PSGL-1 regulate Th1 cell infiltration, resulting in the inhibition of fibrosis