PMID- 10092216
OWN - NLM
STAT- MEDLINE
DCOM- 19990422
LR  - 20191210
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 177
IP  - 4
DP  - 1998 Dec
TI  - Isolation and characterization of a cDNA clone encoding a novel peptide (OSF)
      that enhances osteoclast formation and bone resorption.
PG  - 636-45
AB  - Using an expression cloning approach, we identified and cloned a novel
      intracellular protein produced by osteoclasts that indirectly induces osteoclast 
      formation and bone resorption, termed OSF. Conditioned media from 293 cells
      transiently transfected with the 0.9 kb OSF cDNA clone stimulated osteoclast-like
      cell formation in both human and murine marrow cultures in the presence or
      absence 10(-9) M 1,25-dihydroxyvitamin D3. In addition, conditioned media from
      293 cells transfected with the OSF cDNA clone enhanced the stimulatory effects of
      1,25-(OH)2D3 on bone resorption in the fetal rat long bone assay. In situ
      hybridization studies using antisense oligomers showed expression of OSF mRNA in 
      highly purified osteoclast-like cells from human giant cell tumors of the bone.
      Northern blot analysis demonstrated ubiquitous expression of a 1.3 kb mRNA that
      encodes OSF in multiple human tissues. Sequence analysis showed the OSF cDNA
      encoded a 28 kD peptide that contains a c-Src homology 3 domain (SH3) and ankyrin
      repeats, suggesting that it was not a secreted protein, but that it was
      potentially involved in cell signaling. Consistent with these data, immunoblot
      analysis using rabbit antisera against recombinant OSF demonstrated OSF
      expression in cell lysates but not in the culture media. Furthermore, recombinant
      OSF had a high affinity for c-Src, an important regulator of osteoclast activity.
      Taken together, these data suggest that OSF is a novel intracellular protein that
      indirectly enhances osteoclast formation and osteoclastic bone resorption through
      the cellular signal transduction cascade, possibly through its interactions with 
      c-Src or other Src-related proteins.
FAU - Reddy, S
AU  - Reddy S
AD  - Department of Medicine/Hematology/Endocrinology, the Veterans Administration
      Medical Center and The University of Texas Health Science Center, San Antonio,
      USA.
FAU - Devlin, R
AU  - Devlin R
FAU - Menaa, C
AU  - Menaa C
FAU - Nishimura, R
AU  - Nishimura R
FAU - Choi, S J
AU  - Choi SJ
FAU - Dallas, M
AU  - Dallas M
FAU - Yoneda, T
AU  - Yoneda T
FAU - Roodman, G D
AU  - Roodman GD
LA  - eng
SI  - GENBANK/U63717
GR  - AG 39529/AG/NIA NIH HHS/United States
GR  - AM 35188/AM/NIADDK NIH HHS/United States
GR  - AR41336/AR/NIAMS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (DNA, Complementary)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (OSTF1 protein, human)
RN  - 0 (Proteins)
RN  - 0 (Recombinant Fusion Proteins)
RN  - EC 2.7.10.2 (src-Family Kinases)
SB  - IM
SB  - S
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Bone Marrow Cells/cytology/drug effects
MH  - Bone Resorption/*genetics
MH  - Cells, Cultured
MH  - Culture Media, Conditioned
MH  - DNA, Complementary/*genetics/isolation & purification
MH  - Gene Expression Regulation
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins
MH  - Mice
MH  - Molecular Sequence Data
MH  - Osteoclasts/*cytology
MH  - Proteins/*genetics/physiology
MH  - Rabbits
MH  - Rats
MH  - Recombinant Fusion Proteins/biosynthesis
MH  - Signal Transduction/physiology
MH  - src Homology Domains
MH  - src-Family Kinases/physiology
EDAT- 1999/03/26 03:03
MHDA- 2000/06/20 09:00
CRDT- 1999/03/26 03:03
PHST- 1999/03/26 03:03 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/03/26 03:03 [entrez]
AID - 10.1002/(SICI)1097-4652(199812)177:4<636::AID-JCP14>3.0.CO;2-H [pii]
AID - 10.1002/(SICI)1097-4652(199812)177:4<636::AID-JCP14>3.0.CO;2-H [doi]
PST - ppublish
SO  - J Cell Physiol. 1998 Dec;177(4):636-45. doi:
      10.1002/(SICI)1097-4652(199812)177:4<636::AID-JCP14>3.0.CO;2-H.