Role of CrkII Signaling in RANKL-Induced Osteoclast Differentiation and Function

No abstract is available for this paper.

• Publication year

  2016

• Venue

  Journal of Immunology

• Publication date

  2016-02-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4049/jimmunol.1501998PMID 26695370
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2013influential reference
• Regulation of osteoclast function

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  2010cited by this paper
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  2009cited by this paper
• Selective inhibition of RANK blocks osteoclast maturation and function and prevents bone loss in mice.

  2009cited by this paper
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  2009cited by this paper
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  2008cited by this paper
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  2007cited by this paper
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  2007cited by this paper
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  2006cited by this paper
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  2005cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2004cited by this paper
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  2003cited by this paper
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  2003cited by this paper
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  2002cited by this paper
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  2001influential reference
• CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration.

  2001cited by this paper
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  2000cited by this paper
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  1998cited by this paper
• Tyrosine Phosphorylation of p130Cas Is Involved in Actin Organization in Osteoclasts*

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  1996cited by this paper
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  1995cited by this paper
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  1995cited by this paper
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  1994cited by this paper
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  1994cited by this paper
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  1993cited by this paper
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  1992cited by this paper
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  1992cited by this paper

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  2020cites this paper
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• Animal Models

  2018cites this paper
• Animal Models: Genetic Manipulation

  2018cites this paper
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  2018cites this paper
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  2017cites this paper