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Mouse (Murine) TNFSF11 Protein expressed in HEK-293 Cells - ABIN1344301
Beleut, Rajaram, Caikovski, Ayyanan, Germano, Choi, Schneider, Brisken: Two distinct mechanisms underlie progesterone-induced proliferation in the mammary gland. in Proceedings of the National Academy of Sciences of the United States of America 2010
RANK is frequently expressed by cancer cells in contrast with RANKL which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review)
Proinsulin (show INS Proteins) C-peptide prevents a reduction of type I collagen expression and decreases, in combination with insulin (show INS Proteins), receptor activator of nuclear factor-kappaB (RANKL) levels.
The RANKL/OPG ratio significantly increased in the presence of bone metastasis with appropriate sensitivity and specificity (73% and 72%, respectively) at a cutoff of >/=0.14 for the detection of bone metastasis. Serum OPG (show TNFRSF11B Proteins) and RANKL/OPG ratios are promising biomarkers for detecting bone metastasis in breast cancer patients.
Correlations between sRANKL and IL-18 (show IL18 Proteins) in BALF.
RANK/RANKL signaling is involved in the androgen deprivation therapy-induced acceleration of bone metastasis in castration-insensitive prostate cancer and is inhibited by osteoprotegerin (show TNFRSF11B Proteins) to prevent bone metastasis.
This study suggested that RANKL could be a marker to differentiate between pagetoid squamous cell carcinoma in situ and extramammary Paget disease .
TNF-alpha-converting enzyme (show ADAM17 Proteins) -mediated cleavage of soluble RANKL from activated lymphocytes, especially B cells, can promote osteoclastogenesis in periodontitis.
RANKL is required for progesterone-mediated cell proliferation in BRCA1mut/+ breast tissue.
MAOA (show MAOA Proteins) provides tumor cell growth advantages in the bone microenvironment by stimulating interleukin-6 (IL6 (show IL6 Proteins)) release from osteoblasts, and triggers skeletal colonization by activating osteoclastogenesis through osteoblast production of RANKL and IL6 (show IL6 Proteins).
In this review, we will provide a summary of the biological functions of RANK signaling pathway (receptor activator of nuclear factor kappaB ligand RANKL and its receptor RANK ) and downstream pathways in bone remodeling, immunity and epithelial homeostasis, with a particular emphasis on cancer
The anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 (show NFATC1 Proteins) activity and the attenuation of RANKL-mediated Ca(2 (show CA2 Proteins)+) signaling as well as NF-kappaB (show NFKB1 Proteins) and MAPK (show MAPK1 Proteins) pathways.
Osteoprotegerin (show TNFRSF11B Proteins) facilitates pulmonary arterial hypertension pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation via integrin alphavbeta3 (show ITGAV Proteins)/FAK (show PTK2 Proteins)/AKT (show AKT1 Proteins) signaling pathway.
results demonstrate that IL-15 (show IL15 Proteins) and RANKL induce osteoclastogenesis synergistically, and IL-15 (show IL15 Proteins) might play a novel and major role in destructive inflammatory bone diseases
Absence of Musashi2 (show MSI2 Proteins) in osteoclast precursors promotes apoptosis and inhibits RANKL-induced NF-kappaB (show NFKB1 Proteins) activation, which is essential for osteoclast survival.
This study demonstrates that Col6a1 (show COL6A1 Proteins)-Cre driver mice are as useful as Twist2 (show TWIST2 Proteins)-Cre driver mice for functional analyses of GALT (show GALT Proteins)-resident mesenchymal cells, including MCi (show MCIN Proteins) cells.
Estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane.
Data suggest that mutations at position I248 in DE-loop of murine RANKL have effects on interaction of RANKL with RANK and on subsequent activation of osteoclastogenesis by this hetero-multimer. (RANKL = osteoclast differentiation factor; RANK = tumor necrosis factor (show TNF Proteins) receptor superfamily, member 11a protein)
sRANKL increased macrophage glucose uptake at normal glucose concentrations, which was impaired by hyperglycemia pretreatment through the inhibition of Glut1 (show SLC2A1 Proteins) membrane translocation and the insulin receptor (show INSR Proteins) and IRS-1 (show IRS1 Proteins) gene transcription.
Our findings show that anti-RANKL antibody administration during pregnancy results in not only an undesirable increase in bone mass, but also has harmful effects on newborn survival.
RANKL represses the transcription of the E3 ubiquitin ligase (show MUL1 Proteins) RNF146 (show RNF146 Proteins) through an NF-kappaB (show NFKB1 Proteins)-related inhibitory element in the RNF146 (show RNF146 Proteins) promoter.
This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.
TNF-related activation-induced cytokine
, osteoclast differentiation factor
, osteoprotegerin ligand
, receptor activator of nuclear factor kappa B ligand
, receptor activator of nuclear factor kappa-B ligand
, tumor necrosis factor ligand superfamily member 11
, tumor necrosis factor (ligand) superfamily, member 11
, Receptor activator of nuclear factor kappa-B ligand
, OPG ligand
, receptor activator of NF-kappaB ligand
, tumor necrosis factor-related activation-induced cytokine
, TNF superfamily member 11 L homeolog
, tumor necrosis factor superfamily member 11 L homeolog