Disease relevance of Ulbp1

• NK cell activation through the NKG2D ligand MULT-1 is selectively prevented by the glycoprotein encoded by mouse cytomegalovirus gene m145 [1].

Psychiatry related information on Ulbp1

• Adult BALB/c mice were injected IP with trimethyltin . HCl (TMT), and the effects of TMT were studied on gross behavior, lethality, spontaneous motor activity (SMA), and responding under a multiple fixed-ratio 30, fixed-interval 600 sec (mult FR30 FI600) schedule of reinforcement [2].

High impact information on Ulbp1

• A distinct N-terminal module within the fcr-1 ectodomain in conjunction with the fcr-1 transmembrane domain was required to dispose MULT-1 to degradation in lysosomes [3].
• Our findings underline the significance of escaping MULT-1/NKG2D signaling for viral survival and maintenance [1].
• The MCMV m145-encoded glycoprotein turned out to be necessary and sufficient to regulate MULT-1 by preventing plasma membrane residence of MULT-1 [1].
• The importance of MULT-1 in NK cell regulation in vivo was confirmed by the attenuating effect of the m145 deletion that was lifted after NK cell depletion [1].
• We set out to define the viral gene product regulating murine UL16-binding protein-like transcript (MULT)-1, a newly described NKG2D ligand [1].

Biological context of Ulbp1

• We show that MCMV infection strongly induces MULT-1 gene expression, but surface expression of this glycoprotein is nevertheless completely abolished by the virus [1].

Associations of Ulbp1 with chemical compounds

• Here we compared the molecular recognition between NKG2D and three of the known ligands, UL16 binding protein (ULBP), MHC class I-like molecule, and retinoic acid early inducible gene as observed in the ligand-complexed crystal structures [4].
• The lowest dose of caffeine, 1 mg/kg, had no effect on responding under either component of the mult schedule [5].
• PIA decreased responding under both components of the mult schedule in a dose-dependent, and similar, manner [5].
• No potency differences were observed between the isomers of pentobarbital and secobarbital on the responding of mice under the mult FR30 FI600 schedule over a dose range of 1-30 mg/kg [6].
• The NMDA antagonist MK-801 at 0.3 mg/kg, i.p. increased the punished response under a MULT VI 1.5/FR 5-punishment schedule of food reinforcement in mice [7].

Other interactions of Ulbp1

• TLR signaling, through the MyD88 adaptor, up-regulates transcription of the retinoic acid early inducible-1 (RAE-1) family of NKG2D ligands, but not H-60 or murine UL16-binding protein-like transcript-1 [8].

References