Cited by 196

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Impaired Micro-RNA Pathways Diminish Osteoclast Differentiation and Function

Sugatani, Toshifumi, Hruska, Keith A.·2009·Journal of Biological Chemistry

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1074/jbc.m805777200

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Figures

FIGURE 1 Gene silencing and function of DGCR8, Dicer1 or Ago2 in osteoclast precursors. Quantitative real time PCR was performed with primer for mouse DGCR8 ( A ), Dicer1 ( B ), or Ago2 ( C ). The data represent the means ± S.D. of three experiments in triplicate. The loss of DGCR8 ( D ), Dicer1 ( E ), or Ago2 ( F ) protein expression levels by siRNA gene silencing was analyzed by immunoblotting ( IB ) using nuclear or whole cell extracts. Quantitative image analysis of these protein expression levels was normalized to GAPDH ( %scr ). scr , scrambled. miRNA RT-PCR ( G and H ) and quantitative real time RT-PCR ( I ) were performed to measure miRNA-223 and miRNA-155 expression levels. The PCR products were confirmed using a 20% polyacrylamide gel, with U6 small nuclear RNA as a loading control ( G and H ). PCR products were normalized to U6 level for each reaction ( I ). The data represent the means ± S.D. of three experiments in triplicate.
FIGURE 1 Gene silencing and function of DGCR8, Dicer1 or Ago2 in osteoclast precursors. Quantitative real time PCR was performed with primer for mouse DGCR8 ( A ), Dicer1 ( B ), or Ago2 ( C ). The data represent the means ± S.D. of three experiments in triplicate. The loss of DGCR8 ( D ), Dicer1 ( E ), or Ago2 ( F ) protein expression levels by siRNA gene silencing was analyzed by immunoblotting ( IB ) using nuclear or whole cell extracts. Quantitative image analysis of these protein expression levels was normalized to GAPDH ( %scr ). scr , scrambled. miRNA RT-PCR ( G and H ) and quantitative real time RT-PCR ( I ) were performed to measure miRNA-223 and miRNA-155 expression levels. The PCR products were confirmed using a 20% polyacrylamide gel, with U6 small nuclear RNA as a loading control ( G and H ). PCR products were normalized to U6 level for each reaction ( I ). The data represent the means ± S.D. of three experiments in triplicate.CC-BY · From the PDF
FIGURE 2 Expression of transcription factors in osteoclast differentiation. Infected cells were treated with RANKL (50 ng/ml) for 3 days, and nuclear extracts were analyzed by immunoblotting with antibodies against PU.1( A ), MITF ( B ), c-Fos ( C ), and NFATc1 ( D ). Quantitative image analysis of the protein expression levels (values below bands) was normalized to histone H3. IB , immunoblotting.
FIGURE 2 Expression of transcription factors in osteoclast differentiation. Infected cells were treated with RANKL (50 ng/ml) for 3 days, and nuclear extracts were analyzed by immunoblotting with antibodies against PU.1( A ), MITF ( B ), c-Fos ( C ), and NFATc1 ( D ). Quantitative image analysis of the protein expression levels (values below bands) was normalized to histone H3. IB , immunoblotting.CC-BY · From the PDF
FIGURE 3 ChIP analysis. ShownareChIPassays to study the association of NFATc1, c-Fos, PU.1, and MITF with NFATc1 or TRAP promoters during osteoclast differentiation with RANKL (50 ng/ml) stimulation for indicated times.
FIGURE 3 ChIP analysis. ShownareChIPassays to study the association of NFATc1, c-Fos, PU.1, and MITF with NFATc1 or TRAP promoters during osteoclast differentiation with RANKL (50 ng/ml) stimulation for indicated times.CC-BY · From the PDF
Image 4
CC-BY · From the PDF
Image 5
CC-BY · From the PDF
Image 6
CC-BY · From the PDF
Image 7
CC-BY · From the PDF
FIGURE 8 Inhibition of miRNA-223 expression causes aberrant osteoclastogenesis. A and B , RAW264.7 cells were transiently transfected with antisense miRNA-223ornegativecontrololigonucleotides,andthecellsweretreatedwithRANKL(100ng/ml).After5days,thecellswerethenfixedandstainedforTRAP, and the number of TRAP-positive multinucleated cells was scored. Similar findings were obtained in four independent sets of experiments. C and D , NFI-A, M-CSFR,andPU.1levelsinRAW264.7cellswithnegativecontrolorantisensemiRNA-223andinfectedosteoclastprecursorswereanalyzedbyimmunoblotting ( IB ) using whole cell extracts. Quantitative image analyses of these protein expression levels were normalized to GAPDH. D , The expression levels of miRNA-223 was measured by miRNA Northern blotting using biotin prelabeled probes specific for miRNA-223. Sno234 was used as a loading control. The sno234 normalized fold increase in the miRNA-223 in osteoclast precursors with pMX-PU.1 retroviral vector is shown.
FIGURE 8 Inhibition of miRNA-223 expression causes aberrant osteoclastogenesis. A and B , RAW264.7 cells were transiently transfected with antisense miRNA-223ornegativecontrololigonucleotides,andthecellsweretreatedwithRANKL(100ng/ml).After5days,thecellswerethenfixedandstainedforTRAP, and the number of TRAP-positive multinucleated cells was scored. Similar findings were obtained in four independent sets of experiments. C and D , NFI-A, M-CSFR,andPU.1levelsinRAW264.7cellswithnegativecontrolorantisensemiRNA-223andinfectedosteoclastprecursorswereanalyzedbyimmunoblotting ( IB ) using whole cell extracts. Quantitative image analyses of these protein expression levels were normalized to GAPDH. D , The expression levels of miRNA-223 was measured by miRNA Northern blotting using biotin prelabeled probes specific for miRNA-223. Sno234 was used as a loading control. The sno234 normalized fold increase in the miRNA-223 in osteoclast precursors with pMX-PU.1 retroviral vector is shown.CC-BY · From the PDF
FIGURE9 Amodelofanovelmechanismforcontrollingosteoclastdifferentiation and function by miRNA-223 in osteoclast precursors. PU.1 induced by M-CSF activates the transcription of miRNA-223, which causes a negative control on M-CSFR expression levels. Also, induced PU.1 stimulates RANK expression, and consequently osteoclast differentiation and function are induced by M-CSF and RANKL stimulation.
FIGURE9 Amodelofanovelmechanismforcontrollingosteoclastdifferentiation and function by miRNA-223 in osteoclast precursors. PU.1 induced by M-CSF activates the transcription of miRNA-223, which causes a negative control on M-CSFR expression levels. Also, induced PU.1 stimulates RANK expression, and consequently osteoclast differentiation and function are induced by M-CSF and RANKL stimulation.CC-BY · From the PDF

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 43

  1. Karsenty, 2002, Dev. Cell., 2, 389, 10.1016/S1534-5807(02)00157-0 · DOI
  2. Tanaka, 2005, Immunol. Rev., 208, 30, 10.1111/j.0105-2896.2005.00327.x · DOI
  3. Del, 2008, Arch. Biochem. Biophys., 473, 147, 10.1016/j.abb.2008.01.011 · DOI
  4. Tondravi, 1997, Nature., 386, 81, 10.1038/386081a0 · DOI
  5. Grigoriadis, 1994, Science., 266, 443, 10.1126/science.7939685 · DOI
  6. Iotsova, 1997, Nat. Med., 3, 1285, 10.1038/nm1197-1285 · DOI
  7. Franzoso, 1997, Genes Dev., 11, 3482, 10.1101/gad.11.24.3482 · DOI · Paper page
  8. Weilbaecher, 2001, Mol. Cell., 8, 749, 10.1016/S1097-2765(01)00360-4 · DOI
  9. Kim, 2005, Nat. Rev. Mol. Cell. Biol., 6, 376, 10.1038/nrm1644 · DOI · Paper page
  10. Lagos-Quintana, 2001, Science., 294, 853, 10.1126/science.1064921 · DOI · Paper page
  11. Lau, 2001, Science., 294, 858, 10.1126/science.1065062 · DOI · Paper page
  12. Lee, 2001, Science., 294, 862, 10.1126/science.1065329 · DOI · Paper page
  13. Bushati, 2007, Annu. Rev. Cell Dev. Biol., 23, 175, 10.1146/annurev.cellbio.23.090506.123406 · DOI · Paper page
  14. Bernstein, 2001, Nature., 409, 363, 10.1038/35053110 · DOI
  15. Hammond, 2001, Science., 293, 1146, 10.1126/science.1064023 · DOI · Paper page
  16. Chen, 2004, Science., 303, 83, 10.1126/science.1091903 · DOI · Paper page
  17. Fukao, 2007, Cell., 129, 617, 10.1016/j.cell.2007.02.048 · DOI · Paper page
  18. Zhou, 2007, Proc. Natl. Acad. Sci. U. S. A., 104, 7080, 10.1073/pnas.0702409104 · DOI
  19. Costinean, 2006, Proc. Natl. Acad. Sci. U. S. A., 103, 7024, 10.1073/pnas.0602266103 · DOI
  20. Sugatani, 2007, J. Cell. Biochem., 101, 996, 10.1002/jcb.21335 · DOI
  21. Luzi, 2008, J. Bone Miner. Res., 23, 287, 10.1359/jbmr.071011 · DOI
  22. Mizuno, 2008, Biochem. Biophys. Res. Commun., 368, 267, 10.1016/j.bbrc.2008.01.073 · DOI
  23. Kobayashi, 2008, Proc. Natl. Acad. Sci. U. S. A., 105, 1949, 10.1073/pnas.0707900105 · DOI
  24. Takeshita, 2000, J. Bone Miner. Res., 15, 1477, 10.1359/jbmr.2000.15.8.1477 · DOI
  25. Harfe, 2005, Proc. Natl. Acad. Sci. U. S. A., 102, 10898, 10.1073/pnas.0504834102 · DOI
  26. Ferron, 2005, Genesis., 41, 138, 10.1002/gene.20108 · DOI
  27. O'Carroll, 2007, Genes Dev., 21, 1999, 10.1101/gad.1565607 · DOI
  28. Matsuo, 2004, J. Biol. Chem., 279, 26475, 10.1074/jbc.M313973200 · DOI
  29. Matsumoto, 2004, J. Biol. Chem., 279, 45969, 10.1074/jbc.M408795200 · DOI · Paper page
  30. Sundaram, 2007, Exp. Cell Res., 313, 168, 10.1016/j.yexcr.2006.10.001 · DOI
  31. Crotti, 2006, Gene (Amst.)., 372, 92, 10.1016/j.gene.2005.12.012 · DOI
  32. Sharma, 2007, J. Biol. Chem., 282, 15921, 10.1074/jbc.M609723200 · DOI
  33. Hu, 2007, Mol. Cell. Biol., 27, 4018, 10.1128/MCB.01839-06 · DOI · Paper page
  34. Pang, 2007, Gene (Amst.)., 403, 151, 10.1016/j.gene.2007.08.007 · DOI
  35. Shen, 2007, Biochim. Biophys. Acta., 1769, 659, 10.1016/j.bbaexp.2007.08.005 · DOI
  36. Asagiri, 2007, Bone., 40, 251, 10.1016/j.bone.2006.09.023 · DOI · Paper page
  37. Walsh, 2003, Gene (Amst.)., 307, 111, 10.1016/S0378-1119(03)00449-9 · DOI
  38. Rosa, 2007, Proc. Natl. Acad. Sci. U. S. A., 104, 19849, 10.1073/pnas.0706963104 · DOI · Paper page
  39. Kwon, 2005, Biochem. Biophys. Res. Commun., 335, 437, 10.1016/j.bbrc.2005.07.092 · DOI
  40. Dougall, 1999, Genes Dev., 13, 2412, 10.1101/gad.13.18.2412 · DOI · Paper page
  41. Diederichs, 2007, Cell., 131, 1097, 10.1016/j.cell.2007.10.032 · DOI
  42. Gregory, 2005, Cell., 123, 631, 10.1016/j.cell.2005.10.022 · DOI · Paper page
  43. Vigorito, 2007, Immunity., 27, 847, 10.1016/j.immuni.2007.10.009 · DOI

Cited by

Sorted by citations

See all 196

Metadata

Authors
Sugatani, T., & Hruska, K. A.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2009-02
Volume
284
Issue
7
Pages
4667-4678
ISSN
0021-9258
Cited by
196
References
6
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review