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The protein encoded by FBLN5 is a secreted, extracellular matrix protein containing an Arg-Gly-Asp (RGD) motif and calcium-binding EGF-like domains. Additionally we are shipping Fibulin 5 Antibodies (149) and Fibulin 5 Proteins (15) and many more products for this protein.
Showing 10 out of 41 products:
Rat (Rattus) Fibulin 5 ELISA Kit for Sandwich ELISA - ABIN814661
Guo, Cheng, Chen, Xing, Xu, Feng, Qin: Overexpression of Fibulin-5 Attenuates Ischemia/Reperfusion Injury After Middle Cerebral Artery Occlusion in Rats. in Molecular neurobiology 2015
Human Fibulin 5 ELISA Kit for Sandwich ELISA - ABIN415297
Hu, Dong, Zhao, Xu, Qin: Fibulin-5: a novel biomarker for evaluating severity and predicting prognosis in patients with acute intracerebral haemorrhage. in European journal of neurology 2016
study reports the first Chinese family with c.1117C>T mutation of FBLN5; findings confirm a novel subtype of autosomal-dominant Charcot-Marie-Tooth disease due to a mutation in the FBLN5 gene
The results showed a significant upregulation of ECM1 (show ECM1 ELISA Kits) and ITGB3 (show ITGB3 ELISA Kits), and a significant downregulation for FBLN5 in pelvic organ prolapse patients.
Serum fibulin-5 concentration can be regarded as a biomarker for evaluating disease severity and predicting prognosis in intracerebral hemorrhage patients.
Fibulin-5 expression is increased in the induced sputum of asthmatic patients.
Data show that fibulin-5 strongly binds to the endothelial cell surface reducing endothelial cell viability and interfering with the signaling pathways of the Ang-1 (show ANGPT1 ELISA Kits)/TIE-2 (show TEK ELISA Kits) receptor axis.
FBLN5 downregulation in human abdominal aortic aneurysm could contribute to extracellular matrix remodeling induced by the inflammatory component of the disease.
Identify a SOX9 (show SOX9 ELISA Kits)/HDAC (show HDAC3 ELISA Kits)-dependent mechanism involved in the down-regulation of FBLN5 by inflammation in abdominal aortic aneurysms.
We also found that Fibulin-5 reduces the level of expression of Ki-67 (show MKI67 ELISA Kits), a nuclear protein associated with cell proliferation. Moreover, reduction in Fibulin-5 expression corresponds to an increase of Ki-67 (show MKI67 ELISA Kits) detection in breast tissue samples
study demonstrates the pivotal role of the extracellular protein, fibulin-5, on the adhesion and proliferation of human keloid-derived cells, through binding to integrin beta-1 (show ITGB1 ELISA Kits)
Lower FBLN-5 expression is an important indicator of poor survival in hepatocellular carcinoma. FBLN-5 inhibits HCC adhesion/motility via integrin-dependent mechanism.
Fibulin-5 overexpression promoted the proliferation and migration of airway smooth muscle cell.
Fibulin-5 overexpression significantly down-regulated the phosphorylation level of eIF2alpha (show EIF2A ELISA Kits) and subsequently inhibited the TRPV1 (show TRPV1 ELISA Kits) channel and CREB (show CREB1 ELISA Kits)/CGRP (show CALCA ELISA Kits) signaling
therapy-induced hypoxia elevated Fbln5 expression, whereas pharmacologic inhibition of TGF-beta (show TGFB1 ELISA Kits) signaling reduced Fbln5 expression. These findings offer insight into the signaling axis that induces Fbln5 expression in PDA and a potential strategy to block its production
Data indicate that Fbln5 promotes PDAC progression by functioning as a molecular rheostat that modulates cell-ECM (show MMRN1 ELISA Kits) interactions to reduce ROS (show ROS1 ELISA Kits) production, and thus tip the balance in favor of tumor cell survival and treatment-refractory disease.
While premaxillo-maxillary suture mesenchymal cells in fibulin-5-null mice were capable of differentiating into osteoblasts, suture cells in mutant mice were less proliferative.
Fibulin-5 plays critical roles in proliferation, migration and invasion of certain tumors, and the effect of fibulin-5 on tumorigenesis appears to be largely context-dependent. (Review)
These results are consistent with a role for TGFbeta2 in lung septation and for Ltbp4 (show LTBP4 ELISA Kits) in regulating fibulin-5 dependent elastic fiber assembly.
Without LTBP-4 (show LTBP4 ELISA Kits), fibulin-5 and tropoelastin (show ELN ELISA Kits) deposition was discontinuous and punctate in vitro and in vivo
This study used the maturation of fibulin-5 knockout (KO) and wild-type mice to study the effects of fragmented elastic fibers on the growth and remodeling of carotid arteries.
These results suggest a novel regulatory mechanism of elastic fiber assembly in which LTBP-2 (show LTBP2 ELISA Kits) regulates targeting of DANCE on suitable microfibrils to form elastic fibers.
The protein encoded by this gene is a secreted, extracellular matrix protein containing an Arg-Gly-Asp (RGD) motif and calcium-binding EGF-like domains. It promotes adhesion of endothelial cells through interaction of integrins and the RGD motif. It is prominently expressed in developing arteries but less so in adult vessels. However, its expression is reinduced in balloon-injured vessels and atherosclerotic lesions, notably in intimal vascular smooth muscle cells and endothelial cells. Therefore, the protein encoded by this gene may play a role in vascular development and remodeling. Defects in this gene are a cause of autosomal dominant cutis laxa, autosomal recessive cutis laxa type I (CL type I), and age-related macular degeneration type 3 (ARMD3).
, fibulin 5
, developmental arteries and neural crest EGF-like protein
, urine p50 protein
, embryonic vascular EGF repeat-containing protein