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IGFBP-7 was lower in heart failure with a preserved ejection fraction than heart failure with a reduced ejection fraction.
IGFBP7 is associated to prognosis and could suppress cell survival in cholangiocarcinoma
Study results demonstrate that urinary TIMP-2*IGFBP-7 concentration can be used in infants to predict subsequent serum creatinine-defined acute kidney injury following cardiopulmonary bypass.
Placenta and appetite genes GDF15 and IGFBP7 are associated with hyperemesis gravidarum.
IGFBP7 upregulation promotes osteogenic differentiation of mesenchymal stem cells via the Wnt/beta-catenin signaling.
Low IGFBP7 expression is associated with Gastric Cancer.
Reduced RNA editing of IGFBP7 gene is associated with psoriasis.
Urine levels of IGFBP7 (and TIMP2) are predictive for acute kidney injury following cardiac surgical procedures.
IGFBPrP1 transfection inhibited cell growth, and induced G1 phase arrest and cellular senescence in HEC1A cells while gene silencing presented the adverse functional changes.
Serum IGFBP7 levels were raised during acute exacerbation in COPD patients.
biomarker for acute kidney injury
epithelial cells and leukocytes from the urinary sediment. CONCLUSION: The gene expression pattern of IGFBP7 and TIMP-2 from urinary sediment, which contains desquamated renal tubular epithelial cells, did not correlate with [IGFBP7]x[TIMP-2] protein, indicating that IGFBP7 and TIMP-2 measured in the NephroCheck(R) test originated predominantly from intact but stressed cells of the kidney itself
In patients with heart failure with preserved ejection fraction, IGFBP7 may be a novel biomarker of diastolic function and exercise capacity.
High IGFBP7 expression is associated with acute kidney injury.
NEAT1-associated paraspeckle proteins P54nrb and PSF have been reported as positive regulators of c-Myc translation through interaction with c-Myc IRES
Urine [TIMP-2]*[IGFBP7] is a promising candidate for early detection of AKI, especially in ruling-out AKI
Meta-analysis indicated that urinary [TIMP-2].[IGFBP7] may be a reliable biomarker for the early detection of acute kidney injury in adults.
TIMP-2 is both expressed and secreted preferentially by cells of distal tubule origin, while IGFBP7 is equally expressed across tubule cell types yet preferentially secreted by cells of proximal tubule origin. In human kidney tissue, strong staining of IGFBP7 was seen in the luminal brush-border region of a subset of proximal tubule cells, and TIMP-2 stained intracellularly in distal tubules.
loss of IGFBP7 and upregulation of IGF1 activates the FGF4-FGFR1-ETS2 pathway in Tumor-associated endothelial cells (TECs) and converts naive tumor cells to chemoresistant tumor stem-like cells (TSCs), thereby facilitating their invasiveness and progression.
study of polymorphisms of the porcine IGFBP7 promoter region in different pig breeds
analysis of how A-to-I RNA editing of the IGFBP7 transcript increases during aging in porcine brain tissues
Our findings define an immune component of the pleiotropic mechanisms through which IGFBP7 suppresses hepatocellular carcinoma
Study shows that IGFBP7 contributes significantly to mesenchymal stromal cells (MSC)-mediated immune modulation, as is shown by decreasing ability of IGFBP7 knockdown in MSCs to restore proliferation and cytokine production in T-cells.
data suggest that IGFBP-7 was up regulated during EAE and inhibit the transition from OPCs to mature OLs, implying its use as a potential therapeutic target for the treatment of inflammatory demyelinating diseases
Our data suggest that loss of Igfbp7 induces precocious involution possibly through diminished cell survival signals.
Angiomodulin is necessary for cardiac commitment of embryonic stem cells (ESCs) and its regulation depends on TAp63 isoform.
results show that Smarcb1 is required for transcriptional activation of Igfbp7 and show that re-introduction of Igfbp7 alone can hinder tumor development; results define a novel mechanism for Smarcb1-mediated tumorigenesis
a model whereby IGFBP7 binds to unoccupied IGF1R and suppresses downstream signaling, thereby inhibiting protein synthesis, cell growth, and survival.
IGFBP7 has a novel role in mouse uterus: it is regulating uterine receptivity through Th1/Th2 lymphocyte balance and decidualization.
fear extinction-induced IGF2/IGFBP7 signalling promotes the survival of 17-19-day-old newborn hippocampal neurons
Results demonstrate that the vascular-specific marker angiomodulin (AGM) modulates vascular remodeling in part by temporizing the proangiogenic effects of VEGF-A.
study showed that IGFBP-rP1 (IGFBP7) was expressed in dysregulated podocytes in a human immunodeficiency virus-associated nephropathy model and in immature podocytes in the developing kidney; conclude that IGFBP-rP1 may be a product of injured podocytes
inhibition of Malignant melanoma growth is due to apoptosis and reduced expression of VEGF induced by pEGFC1-IGFBP7
Mac25 interacts with the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including high endothelial venules, as well as with chemokines implicated in regulation of lymphocyte trafficking, e.g., SLC and IP-10.
Proteolytic processing of mac25 modulates its insulin/IGF-1-dependent growth-stimulatory activity.
IGFBP-7 can regulate glioma cell migration through the AKT-ERK pathway, thereby playing an important role in glioma growth and migration
This gene encodes a member of the insulin-like growth factor (IGF)-binding protein (IGFBP) family. IGFBPs bind IGFs with high affinity, and regulate IGF availability in body fluids and tissues and modulate IGF binding to its receptors. This protein binds IGF-I and IGF-II with relatively low affinity, and belongs to a subfamily of low-affinity IGFBPs. It also stimulates prostacyclin production and cell adhesion. Alternatively spliced transcript variants encoding different isoforms have been described for this gene, and one variant has been associated with retinal arterial macroaneurysm (PMID:21835307).
insulin-like growth factor-binding protein 7
, IGF-binding protein 7
, PGI2-stimulating factor
, prostacyclin-stimulating factor
, tumor-derived adhesion factor