PMID- 10640743
OWN - NLM
STAT- MEDLINE
DCOM- 20000224
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 164
IP  - 3
DP  - 2000 Feb 1
TI  - CCR9A and CCR9B: two receptors for the chemokine CCL25/TECK/Ck beta-15 that
      differ in their sensitivities to ligand.
PG  - 1293-305
AB  - We isolated cDNAs for a chemokine receptor-related protein having the database
      designation GPR-9-6. Two classes of cDNAs were identified from mRNAs that arose
      by alternative splicing and that encode receptors that we refer to as CCR9A and
      CCR9B. CCR9A is predicted to contain 12 additional amino acids at its N terminus 
      as compared with CCR9B. Cells transfected with cDNAs for CCR9A and CCR9B
      responded to the chemokine CC chemokine ligand 25 (CCL25)/thymus-expressed
      chemokine (TECK)/chemokine beta-15 (CK beta-15) in assays for both calcium flux
      and chemotaxis. No other chemokines tested produced responses specific for the
      cDNA-transfected cells. mRNA for CCR9A/B is expressed predominantly in the
      thymus, coincident with the expression of CCL25, and highest expression for
      CCR9A/B among thymocyte subsets was found in CD4+CD8+ cells. mRNAs encoding the A
      and B forms of the receptor were expressed at a ratio of approximately 10:1 in
      immortalized T cell lines, in PBMC, and in diverse populations of thymocytes. The
      EC50 of CCL25 for CCR9A was lower than that for CCR9B, and CCR9A was desensitized
      by doses of CCL25 that failed to silence CCR9B. CCR9 is the first example of a
      chemokine receptor in which alternative mRNA splicing leads to proteins of
      differing activities, providing a mechanism for extending the range of
      concentrations over which a cell can respond to increments in the concentration
      of ligand. The study of CCR9A and CCR9B should enhance our understanding of the
      role of the chemokine system in T cell biology, particularly during the stages of
      thymocyte development.
FAU - Yu, C R
AU  - Yu CR
AD  - Laboratory of Clinical Investigation, National Institute of Allergy and
      Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
FAU - Peden, K W
AU  - Peden KW
FAU - Zaitseva, M B
AU  - Zaitseva MB
FAU - Golding, H
AU  - Golding H
FAU - Farber, J M
AU  - Farber JM
LA  - eng
SI  - GENBANK/AF145439
SI  - GENBANK/AF145440
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (CC chemokine receptor 9)
RN  - 0 (CCL25 protein, human)
RN  - 0 (Chemokines, CC)
RN  - 0 (DNA, Complementary)
RN  - 0 (Ligands)
RN  - 0 (Protein Isoforms)
RN  - 0 (Receptors, CCR)
RN  - 0 (Receptors, Chemokine)
SB  - AIM
SB  - IM
MH  - Alternative Splicing/immunology
MH  - Amino Acid Sequence
MH  - Cell Line
MH  - Cell Movement/genetics/immunology
MH  - Chemokines, CC/*metabolism
MH  - DNA, Complementary/chemistry/isolation & purification
MH  - Gene Expression Regulation/immunology
MH  - Humans
MH  - Jurkat Cells
MH  - Ligands
MH  - Molecular Sequence Data
MH  - Protein Isoforms/genetics/isolation & purification/metabolism/physiology
MH  - Receptors, CCR
MH  - Receptors, Chemokine/genetics/isolation & purification/*metabolism/physiology
MH  - Signal Transduction/genetics/immunology
MH  - Thymus Gland/metabolism
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 2000/01/21 09:00
MHDA- 2000/02/26 09:00
CRDT- 2000/01/21 09:00
PHST- 2000/01/21 09:00 [pubmed]
PHST- 2000/02/26 09:00 [medline]
PHST- 2000/01/21 09:00 [entrez]
AID - ji_v164n3p1293 [pii]
AID - 10.4049/jimmunol.164.3.1293 [doi]
PST - ppublish
SO  - J Immunol. 2000 Feb 1;164(3):1293-305. doi: 10.4049/jimmunol.164.3.1293.