PMID- 15240381
OWN - NLM
STAT- MEDLINE
DCOM- 20040818
LR  - 20081121
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 1018
DP  - 2004 Jun
TI  - Regulation of vasopressin V1b receptors and stress adaptation.
PG  - 293-301
AB  - Vasopressin (VP) regulates pituitary corticotroph function by acting upon plasma 
      membrane G-protein receptors of the V1b subtype (V1bR), coupled to 
      calcium-phospholipid signaling. The number of these receptors in the anterior 
      pituitary varies during stress in direct correlation with corticotroph 
      responsiveness, suggesting that the V1bR plays an important role during 
      adaptation of the hypothalamic-pituitary-adrenal (HPA) axis to stress. The 
      molecular regulation of pituitary V1bR involves transcriptional and translational 
      mechanisms. V1bR gene transcription, which is necessary to maintain V1bR mRNA 
      levels, depends on a number of responsive elements in the promoter region, of 
      which the stretch of GA repeats near the transcription start point (GAGA box) is 
      essential. Although transcriptional activation is necessary to maintain V1bR mRNA 
      levels, the lack of correlation between VP binding and V1bR mRNA suggests that 
      V1bR content is mainly regulated at the translational level. Two potential 
      mechanisms by which the 5' untranslated region (5'UTR) of the V1bR mediates 
      negative and positive regulation of V1bR translation were identified. This 
      includes the repressor effect of small open reading frames (ORF) present upstream 
      of the main V1bR ORF, and an internal ribosome entry site (IRES), which activates 
      V1bR translation. The existence of multiple loci of regulation for the V1bR at 
      transcriptional and translational levels provides a mechanism to facilitate 
      plasticity of regulation of the number of pituitary vasopressin receptors 
      according to physiological demand.
FAU - Volpi, Simona
AU  - Volpi S
AD  - Section on Endocrine Physiology, Developmental Endocrinology Branch, NICHD, NIH, 
      Bldg. 10, Rm. 10N262, 10 Center Drive MSC 1862, Bethesda, MD 20892-1862, USA.
FAU - Rabadan-Diehl, Cristina
AU  - Rabadan-Diehl C
FAU - Aguilera, Greti
AU  - Aguilera G
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Vasopressin)
SB  - IM
MH  - *Adaptation, Physiological
MH  - Animals
MH  - Gene Expression Regulation
MH  - RNA Processing, Post-Transcriptional
MH  - RNA, Messenger/genetics
MH  - Receptors, Vasopressin/genetics/metabolism/*physiology
MH  - Stress, Physiological/*physiopathology
MH  - Transcription, Genetic
RF  - 36
EDAT- 2004/07/09 05:00
MHDA- 2004/08/19 05:00
CRDT- 2004/07/09 05:00
PHST- 2004/07/09 05:00 [pubmed]
PHST- 2004/08/19 05:00 [medline]
PHST- 2004/07/09 05:00 [entrez]
AID - 1018/1/293 [pii]
AID - 10.1196/annals.1296.035 [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2004 Jun;1018:293-301. doi: 10.1196/annals.1296.035.