PMID- 10601355
OWN - NLM
STAT- MEDLINE
DCOM- 20000128
LR  - 20200409
IS  - 0022-1007 (Print)
IS  - 0022-1007 (Linking)
VI  - 190
IP  - 12
DP  - 1999 Dec 20
TI  - Recognition of the class Ib molecule Qa-1(b) by putative activating receptors
      CD94/NKG2C and CD94/NKG2E on mouse natural killer cells.
PG  - 1801-12
AB  - The heterodimeric CD94/NKG2A receptor, expressed by mouse natural killer (NK)
      cells, transduces inhibitory signals upon recognition of its ligand, Qa-1(b), a
      nonclassical major histocompatibility complex class Ib molecule. Here we clone
      and express two additional receptors, CD94/NKG2C and CD94/NKG2E, which we show
      also bind to Qa-1(b). Within their extracellular carbohydrate recognition
      domains, NKG2C and NKG2E share extensive homology with NKG2A (93-95% amino acid
      similarity); however, NKG2C/E receptors differ from NKG2A in their cytoplasmic
      domains (only 33% similarity) and contain features that suggest that CD94/NKG2C
      and CD94/NKG2E may be activating receptors. We employ a novel blocking anti-NKG2 
      monoclonal antibody to provide the first direct evidence that CD94/NKG2 molecules
      are the only Qa-1(b) receptors on NK cells. Molecular analysis reveals that NKG2C
      and NKG2E messages are extensively alternatively spliced and approximately
      20-fold less abundant than NKG2A message in NK cells. The organization of the
      mouse Cd94/Nkg2 gene cluster, presented here, shows striking similarity with that
      of the human, arguing that the entire CD94/NKG2 receptor system is relatively
      primitive in origin. Analysis of synonymous substitution frequencies suggests
      that within a species, NKG2 genes may maintain similarities with each other by
      concerted evolution, possibly involving gene conversion-like events. These
      findings have implications for understanding NK cells and also raise new
      possibilities for the role of Qa-1 in immune responses.
FAU - Vance, R E
AU  - Vance RE
AD  - Department of Molecular Biology, University of California, Berkeley, California
      94720, USA.
FAU - Jamieson, A M
AU  - Jamieson AM
FAU - Raulet, D H
AU  - Raulet DH
LA  - eng
SI  - GENBANK/AF195779
GR  - R01 AI035021/AI/NIAID NIH HHS/United States
GR  - R01-AI35021/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Antigens, CD)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (KLRC1 protein, human)
RN  - 0 (KLRC2 protein, human)
RN  - 0 (KLRC3 protein, human)
RN  - 0 (KLRD1 protein, human)
RN  - 0 (Klrc1 protein, mouse)
RN  - 0 (Klrc2 protein, mouse)
RN  - 0 (Klrc3 protein, mouse)
RN  - 0 (Klrd1 protein, mouse)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Ligands)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NK Cell Lectin-Like Receptor Subfamily C)
RN  - 0 (NK Cell Lectin-Like Receptor Subfamily D)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Natural Killer Cell)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Antigens, CD/*physiology
MH  - CHO Cells
MH  - Cloning, Molecular
MH  - Cricetinae
MH  - Histocompatibility Antigens Class I/*physiology
MH  - Humans
MH  - Killer Cells, Natural/*physiology
MH  - *Lectins, C-Type
MH  - Ligands
MH  - Membrane Glycoproteins/*physiology
MH  - Mice
MH  - Molecular Sequence Data
MH  - NK Cell Lectin-Like Receptor Subfamily C
MH  - NK Cell Lectin-Like Receptor Subfamily D
MH  - Receptors, Immunologic/*physiology
MH  - Receptors, Natural Killer Cell
MH  - Sequence Alignment
PMC - PMC2195720
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - 10.1084/jem.190.12.1801 [doi]
PST - ppublish
SO  - J Exp Med. 1999 Dec 20;190(12):1801-12. doi: 10.1084/jem.190.12.1801.