PMID- 16001330
OWN - NLM
STAT- MEDLINE
DCOM- 20050929
LR  - 20090219
IS  - 0018-5043 (Print)
IS  - 0018-5043 (Linking)
VI  - 37
IP  - 6
DP  - 2005 Jun
TI  - Menin and TGF-beta superfamily member signaling via the Smad pathway in 
      pituitary, parathyroid and osteoblast.
PG  - 375-9
AB  - PITUITARY: Menin is a Smad3-interacting protein; inactivation of menin blocks 
      transforming growth factor (TGF)-beta and activin signaling, antagonizing their 
      growth-inhibitory properties in anterior pituitary cells. Menin is also required 
      for the activin-induced inhibition of prolactin expression mediated by the Smads 
      and the transcription factor, Pit-1. The interaction between menin and Smad3 is 
      direct. PARATHYROID: In cultured parathyroid cells from uremic hemodialysis 
      patients, in which the menin signaling pathways are probably still intact, menin 
      inactivation achieved by menin antisense oligonucleotides leads to loss of 
      TGF-beta inhibition of parathyroid cell proliferation and parathyroid hormone 
      (PTH) secretion. Moreover, TGF-beta does not affect the proliferation and PTH 
      production of parathyroid cells from multiple endocrine neoplasia type 1 (MEN1) 
      patients. OSTEOBLAST: Men1-null mouse fetuses that die at day 12 or earlier have 
      cranial/facial hypoplasias implicating menin in bone development. Menin is 
      required for the commitment of multipotential mesenchymal stem cells into the 
      osteoblast lineage. This is achieved by menin interacting physically and 
      functionally with bone morphogenetic protein (BMP)-2 regulated Smads, such as 
      Smad1 and Smad5, and the key osteoblast regulator, Runx2. These interactions are 
      lost as the committed osteoblasts differentiate further at which time menin 
      interacts with Smad3, mediating the negative regulation of Runx2 by TGF-beta. 
      Menin also suppresses osteoblast maturation, partly by inhibiting the 
      differentiation actions of JunD.
FAU - Hendy, G N
AU  - Hendy GN
AD  - Department of Medicine, Physiology and Human Genetics, McGill University, and 
      Calcium Research Laboratory and Hormones and Cancer Research Unit, Royal Victoria 
      Hospital, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1. 
      geoffrey.hendy@mcgill.ca
FAU - Kaji, H
AU  - Kaji H
FAU - Sowa, H
AU  - Sowa H
FAU - Lebrun, J-J
AU  - Lebrun JJ
FAU - Canaff, L
AU  - Canaff L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Germany
TA  - Horm Metab Res
JT  - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et 
      metabolisme
JID - 0177722
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Men1 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (SMAD1 protein, human)
RN  - 0 (Smad Proteins)
RN  - 0 (Smad1 Protein)
RN  - 0 (Smad1 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Cell Differentiation/genetics
MH  - Cells, Cultured
MH  - DNA-Binding Proteins/*metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Multiple Endocrine Neoplasia Type 1/genetics/metabolism
MH  - Osteoblasts/*metabolism
MH  - Pituitary Gland/*metabolism
MH  - Proto-Oncogene Proteins/genetics
MH  - *Signal Transduction
MH  - Smad Proteins
MH  - Smad1 Protein
MH  - Thyroid Gland/cytology/*metabolism
MH  - Trans-Activators/*metabolism
MH  - Transforming Growth Factor beta/*metabolism
RF  - 49
EDAT- 2005/07/08 09:00
MHDA- 2005/09/30 09:00
CRDT- 2005/07/08 09:00
PHST- 2005/07/08 09:00 [pubmed]
PHST- 2005/09/30 09:00 [medline]
PHST- 2005/07/08 09:00 [entrez]
AID - 10.1055/s-2005-870152 [doi]
PST - ppublish
SO  - Horm Metab Res. 2005 Jun;37(6):375-9. doi: 10.1055/s-2005-870152.