(Q42953444)

English

BAPTA-AM, an intracellular calcium chelator, inhibits RANKL-induced bone marrow macrophages differentiation through MEK/ERK, p38 MAPK and Akt, but not JNK pathways

scientific article published on July 27, 2010

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scholarly article

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Europe PubMed Central

PubMed publication ID

11 November 2017

BAPTA-AM, an intracellular calcium chelator, inhibits RANKL-induced bone marrow macrophages differentiation through MEK/ERK, p38 MAPK and Akt, but not JNK pathways (English)

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Europe PubMed Central

PubMed publication ID

11 November 2017

author name string

Sigui Zhou

1

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Europe PubMed Central

PubMed publication ID

11 November 2017

Xi Yuan

2

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11 November 2017

Qinghua Liu

3

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Europe PubMed Central

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11 November 2017

Xiaoqi Zhang

4

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11 November 2017

Xuediao Pan

5

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11 November 2017

Linquan Zang

6

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11 November 2017

Lipeng Xu

7

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11 November 2017

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27 July 2010

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11 November 2017

full work available at URL

https://api.elsevier.com/content/article/PII:S1043466610001870?httpAccept=text/xml

1 reference

10.1016/J.CYTO.2010.07.003

https://api.crossref.org/works/10.1016/J.CYTO.2010.07.003

12 June 2024

https://api.elsevier.com/content/article/PII:S1043466610001870?httpAccept=text/plain

1 reference

10.1016/J.CYTO.2010.07.003

https://api.crossref.org/works/10.1016/J.CYTO.2010.07.003

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11 November 2017

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11 November 2017

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11 November 2017

210-214

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11 November 2017

Increased myeloid cell responses to M-CSF and RANKL cause bone loss and inflammation in SH3BP2 "cherubism" mice.

1

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The tec family tyrosine kinase Btk Regulates RANKL-induced osteoclast maturation

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Colony-stimulating factor-1 (CSF-1) directly inhibits receptor activator of nuclear factor-{kappa}B ligand (RANKL) expression by osteoblasts

3

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Role of RANKL in bone diseases.

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RANK/RANKL: regulators of immune responses and bone physiology

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MEK/ERK pathway is aberrantly active in Hodgkin disease: a signaling pathway shared by CD30, CD40, and RANK that regulates cell proliferation and survival

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Receptor activator of NF-kappaB (RANK) cytoplasmic motif, 369PFQEP373, plays a predominant role in osteoclast survival in part by activating Akt/PKB and its downstream effector AFX/FOXO4

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Transforming growth factor-beta controls human osteoclastogenesis through the p38 MAPK and regulation of RANK expression

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Membrane depolarization causes a direct activation of G protein-coupled receptors leading to local Ca2+ release in smooth muscle

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Conditional expression of a Gi-coupled receptor in osteoblasts results in trabecular osteopenia

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Alterations of MAPK activities associated with intestinal cell differentiation

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c-Src couples PI 3 kinase/Akt and MAPK signaling to PDGF-induced DNA synthesis in mesangial cells

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A non-disruptive technique for loading calcium buffers and indicators into cells

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Ca2+ controls functional expression of the cardiac K+ transient outward current via the calcineurin pathway

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Ca2+ dependence of the Ca2+-selective TRPV6 channel

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Microtubule disruption with BAPTA and dimethyl BAPTA by a calcium chelation-independent mechanism in 3T3-L1 adipocytes

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Extracellular acidification enhances osteoclast survival through an NFAT-independent, protein kinase C-dependent pathway.

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Calcium/calmodulin-dependent kinase activity is required for efficient induction of osteoclast differentiation and bone resorption by receptor activator of nuclear factor kappa B ligand (RANKL).

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The calcium sensing receptor is directly involved in both osteoclast differentiation and apoptosis

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

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Ca-dependent binding of actin to gelsolin

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Emerging insights into the role of calcium ions in osteoclast regulation

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Beta2-microglobulin stimulates osteoclast formation

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MITF and PU.1 recruit p38 MAPK and NFATc1 to target genes during osteoclast differentiation

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Nitrogen-containing bisphosphonate, YM529/ONO-5920 (a novel minodronic acid), inhibits RANKL expression in a cultured bone marrow stromal cell line ST2.

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Identifiers

10.1016/J.CYTO.2010.07.003

1 reference

Europe PubMed Central

PubMed publication ID

11 November 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

11 November 2017

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