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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. De plus, nous expédions Fibulin 5 Kits (36) et Fibulin 5 Protéines (15) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 140 products:
Human Monoclonal Fibulin 5 Primary Antibody pour IHC, ELISA - ABIN969131
Markova, Zou, Ringpfeil, Sasaki, Kostka, Timpl, Uitto, Chu: Genetic heterogeneity of cutis laxa: a heterozygous tandem duplication within the fibulin-5 (FBLN5) gene. dans American journal of human genetics 2003
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Human Monoclonal Fibulin 5 Primary Antibody pour IHC, ELISA - ABIN969144
Wen, Hochholdinger, Sauer, Bruce, Schnable: The roothairless1 gene of maize encodes a homolog of sec3, which is involved in polar exocytosis. dans Plant physiology 2005
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Human Monoclonal Fibulin 5 Primary Antibody pour ELISA, WB - ABIN969145
Kadoya, Sasaki, Kostka, Timpl, Matsuzaki, Kumagai, Sakai, Nishiyama, Amano: Fibulin-5 deposition in human skin: decrease with ageing and ultraviolet B exposure and increase in solar elastosis. dans The British journal of dermatology 2005
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Human Monoclonal Fibulin 5 Primary Antibody pour EIA, IHC (p) - ABIN1107240
Lee, Roy, Mogford, Schiemann, Mustoe: Fibulin-5 promotes wound healing in vivo. dans Journal of the American College of Surgeons 2004
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Human Polyclonal Fibulin 5 Primary Antibody pour ELISA, WB - ABIN185699
Albig, Neil, Schiemann: Fibulins 3 and 5 antagonize tumor angiogenesis in vivo. dans Cancer research 2006
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 (Montrer ANGPT1 Anticorps)/TIE-2 (Montrer TEK Anticorps) 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 (Montrer SOX9 Anticorps)/HDAC (Montrer HDAC3 Anticorps)-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 (Montrer MKI67 Anticorps), a nuclear protein (Montrer RDBP Anticorps) associated with cell proliferation. Moreover, reduction in Fibulin-5 expression corresponds to an increase of Ki-67 (Montrer MKI67 Anticorps) 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 (Montrer ITGB1 Anticorps)
Lower FBLN-5 expression is an important indicator of poor survival in hepatocellular carcinoma. FBLN-5 inhibits HCC (Montrer FAM126A Anticorps) adhesion/motility via integrin-dependent mechanism.
FBLN5 mRNA expression is upregulated in response to cAMP-mediated decidualization of primary human endometrial stromal cells, although FBLN5 itself does not enhance decidualization
Fibulin-5 is significantly down-regulated in ovarian carcinoma and acts as a tumour suppressor by inhibiting the migration and invasion of ovarian cancer cells.
Data indicate that Fbln5 promotes PDAC progression by functioning as a molecular rheostat that modulates cell-ECM (Montrer MMRN1 Anticorps) interactions to reduce ROS (Montrer ROS1 Anticorps) production, and thus tip the balance in favor of tumor cell survival and treatment-refractory disease.
Data suggest that fibulin-5 functions as a metastasis suppressor in lung cancer by modulating tumor microenvironment to suppress Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) signaling.
Fibulin-5 overexpression significantly down-regulated the phosphorylation level of eIF2alpha (Montrer EIF2A Anticorps) and subsequently inhibited the TRPV1 (Montrer TRPV1 Anticorps) channel and CREB (Montrer CREB1 Anticorps)/CGRP (Montrer CALCA Anticorps) signaling
therapy-induced hypoxia elevated Fbln5 expression, whereas pharmacologic inhibition of TGF-beta (Montrer TGFB1 Anticorps) 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
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 (Montrer LTBP4 Anticorps) in regulating fibulin-5 dependent elastic fiber assembly.
Without LTBP-4 (Montrer LTBP4 Anticorps), fibulin-5 and tropoelastin (Montrer ELN Anticorps) 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.
suggest that uPA (Montrer PLAU Anticorps) promotes cell migration by binding to fibulin-5, initiating its cleavage by plasmin (Montrer PLG Anticorps), which leads to its dissociation from beta1-integrin and thereby unblocks the capacity of integrin to facilitate cell motility
These results suggest a novel regulatory mechanism of elastic fiber assembly in which LTBP-2 (Montrer LTBP2 Anticorps) 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