dc.contributor.author
Damerau, Alexandra
dc.contributor.author
Gaber, Timo
dc.contributor.author
Ohrndorf, Sarah
dc.contributor.author
Hoff, Paula
dc.date.accessioned
2021-01-18T13:12:33Z
dc.date.available
2021-01-18T13:12:33Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/29011
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-28761
dc.description.abstract
The Janus kinase (JAK) signal transducer and activator of transcription (STAT) signaling pathway serves as an important downstream mediator for a variety of cytokines, hormones, and growth factors. Emerging evidence suggests JAK/STAT signaling pathway plays an important role in bone development, metabolism, and healing. In this light, pro-inflammatory cytokines are now clearly implicated in these processes as they can perturb normal bone remodeling through their action on osteoclasts and osteoblasts at both intra- and extra-articular skeletal sites. Here, we summarize the role of JAK/STAT pathway on development, homeostasis, and regeneration based on skeletal phenotype of individual JAK and STAT gene knockout models and selective inhibition of components of the JAK/STAT signaling including influences of JAK inhibition in osteoclasts, osteoblasts, and osteocytes.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
bone development
en
dc.subject
osteoporosis
en
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
9004
dcterms.bibliographicCitation.doi
10.3390/ijms21239004
dcterms.bibliographicCitation.journaltitle
International Journal of Molecular Sciences
dcterms.bibliographicCitation.number
23
dcterms.bibliographicCitation.originalpublishername
MDPI AG
dcterms.bibliographicCitation.volume
21
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
33256266
dcterms.isPartOf.eissn
1422-0067