RANK is the intrinsic hematopoietic cell surface receptor that controls osteoclastogenesis and regulation of bone mass and calcium metabolism.

By Ji Li, I. Sarosi, Xiao-Qiang Yan, S. Morony, C. Capparelli, H. Tan, Susan McCabe, R. Elliott, S. Scully, Gwyneth Van and 13 more. Proceedings of the National Academy of Sciences of the United States of America, 2000

1,176 citations recorded by the source corpus.

Subfields: Sociology and Political Science

View Paper: https://www.semanticscholar.org/paper/87270699f92e636b7670d40002237d617d068a0f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. S. Teitelbaum
2. J. H. Park
3. F. Ross
4. L. Hofbauer
5. Jung-Min Kim
6. N. Lee
7. Soo Young Lee
8. Jonathan D. Lam

Citations in the corpus

• Role of receptor activator of nuclear factor-κB ligand and osteoprotegerin in bone cell biology (2001, background): “However, the fact that RANK-deficient mice are resistant against the hypercalcemic and bone-resorptive effects of IL-1 and TNF-α [38], and that OPG can prevent bone loss in a model of adjuvant arthritis (which is characterized by local overproduction of IL-1 and TNF-α) [11] suggest only a minor and ”
• Osteoclasts: what do they do and how do they do it? (2007, positive): “Although the latter in vitro observation is provocative, the failure of TNF- to induce meaningful osteoclast formation in RANK-deficient mice calls into question the biological relevance of TGF- as a substitute for RANKL.20 On the other hand, there is reasonable evidence that the capacity of TNF- to”
• Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation (2017, background): “Mice with genetic deletions of Tnfsf11 or Tnfrsf11a exhibit severe osteopetrosis accompanied by defective tooth eruption owing to the complete death of their osteoclasts (Dougall et al., 1999; Kong et al., 1999; Li et al., 2000).”
• Genetic regulation of osteoclast development and function (2003, background): “Both Tnfsf11 -knockout mice and mice in which Tnfrsf11a has been deleted (RANK −/− ), fail to generate osteoclasts and are severely osteopetroti”
• Minireview: the OPG/RANKL/RANK system. (2001, background): “Interestingly, similar to the RANKL knockout mice, RANK knockout mice also lacked peripheral lymph nodes and had defective B and T cell maturation but differed from the RANKL knock out mice in having normal thymic development (28).”
• TNF-alpha induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand. (2000, background): “In fact, administration of TNF-α to RANK-deficient animals fails to induce osteoclastogenesis and ameliorate serum hypocalcemia, demonstrating that TNF-α does not substitute for RANKL in physiological conditions (26).”
• Osteoclast differentiation and activation (2003, background): “RANK expression on haematopoietic precursor cells is required in the mouse for osteoclast differentiation and activation, and for the resorption of bone and regulation of calcium homeostasis by calcitropic hormone”
• Changes in proinflammatory cytokine activity after menopause. (2002, background): “Both TNF- (316, 318, 329, 330) and PGE2 (331) may have a direct, RANKL-independent effect on osteoclast differentiation.”
• Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, neutral): “bone resorption (115) or hypercalcemia that was apparent in similarly challenged wild-type mice (63).”