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Rat (Rattus) Polyclonal SULF1 Primary Antibody for WB - ABIN549060
Ai, Do, Lozynska, Kusche-Gullberg, Lindahl, Emerson: QSulf1 remodels the 6-O sulfation states of cell surface heparan sulfate proteoglycans to promote Wnt signaling. in The Journal of cell biology 2003
Show all 4 Pubmed References
High SULF1 expression is associated with glioma.
These findings suggested that SULF1 could be an indicator of the clinicopathological features and prognosis of pancreatic cancer.
Defective autophagy is associated with loss of HSulf-1 in ovarian cancer.
our study found that increased SULF1 expression is significantly predictive of more advanced tumor stage and poorer metastasis-free survival and disease-specific survival in patients with both UTUC and UBUC.
Data show that sulfatase 1 (hSulf-1) overexpression in melanoma cells can inhibit cell proliferation and induce cell cycle arrest and apoptosis by decreasing the protein kinase B (AKT) phosphorylation and limiting cyclin dependent kinase 4 (CDK4) nuclear import.
Sulf-1 is responsive to TNF-alpha stimulation and may function as an autocrine regulator of fibroblast expansion in the course of an inflammatory response
The short variants of Sulf1 promoted FGF2-induced MDA-MB231 and MCF7 in vitro growth while full-length Sulf1 inhibited growth supporting in vivo mammary tumour cell signalling patterns of growth.
The SULF1/SULF2 activation thus does not only promote regulated foetal growth and injury-induced liver regeneration but also dysregulated tumour growth.
Results show that SULF1 or SULF2 overexpression contributes to colorectal cancer cell proliferation, migration, and invasion.
Data suggest that Sulfatase 1 (hSulf-1) may be a suitable target for cancer therapy.
findings show an upregulation of SULF1 in degenerative discs for the first time, and suggest that there is a link between SULF1 and disc degeneration
rs6990375 polymorphism of SULF1 gene could be one of the factors related to recurrent miscarriage in Iranian women.
Loss of HSulf-1 expression promotes tumorigenicity in ovarian cancer through regulating Bim expression.
identification of markers including SULF1 may improve detection of this disease at its earliest stages improving patient treatment and prognosis
SULF1/SULF2 splice variants regulate pancreatic tumor progression.
Knockdown of SULF2 in human corneal epithelial cell line slowed migration, which was restored by overexpression of either mouse SULF2 or human SULF1.
Strong interaction depends on the presence of Sulf1-substrate groups.
Ectopic expression of SULF1 or SULF2 in HeLa cells, which decreases cell surface heparan sulfate proteoglycan sulfation, diminished Chlamydia muridarum binding and decreased vacuole formation.
these observations provide evidence that HPEI nanogels delivering HSulf-1 combined with DDP may have a promising application in the therapy of human ovarian cancer.
miR-21-mediated suppression of both hSulf-1 and PTEN led to activation of AKT/ERK pathways and epithelial-mesenchymal transition in hepatocellular carcinoma, promoting tumor growth.
Sulf1 is required for terminating intestinal stem cell division at the end of regeneration.
vertebrate and Drosophila Sulfs have an intrinsically similar activity and the function of Sulfs in the fate of Wnt/Wg ligands is context-dependent
DSulfatase-1 fine-tunes Hedgehog patterning activity through a novel regulatory feedback loop.
The results demonstrate that sulf1 is a novel Wg target gene and by a feedback mechanism, it negatively regulated Wg signaling and distribution in vivo.
Drosophila heparan sulfate 6-O endosulfatase regulates Wingless morphogen gradient formation
Shh signaling requires the coordinated activity of Sulf1 and Sulf2 in order to reach that threshold in the mouse ventral spinal cord
our findings show that Sulf-1 is an important tumor suppressor gene in hepatocellular carcinoma (HCC), and its over expression downregulates Msln and results in a decrease in HCC cell proliferation, migration, invasion, and lymphatic metastasis.
Sulf1 and Sulf2 play indispensable roles to maintain glomerular integrity and protective roles in diabetic nephropathy, probably by growth factor modulation.
Expression of the heparan sulfate 6-O-endosulfatases, Sulf1 and Sulf2, in the avian and mammalian inner ear suggests a role for sulfation during inner ear development.
Our study proposes a novel role of SULF1 in hepatocellular carcinoma tumor progression through augmentation of the TGF-beta pathway, thus defining SULF1 as a potential biomarker for tumor progression and a novel target for drug development for HCC.
It is proposed that Sulf1, Sulf2 and ErbB1 are involved in the inhibition of neurite outgrowth and may regulate structural plasticity and regeneration in the nervous system.
Sulf1/, but not Sulf2/, mice, exhibited a marked delay in healing of corneal epithelial wounds.
Distinct expression patterns of Sulf1 and Hs6st1 spatially regulate heparan sulfate sulfation during prostate development.
Our study provides additional insights into the temporal control of Olig2 progenitor cell fate change by the identification of Sulf1 as an extracellular timing signal in the ventral spinal cord.
Sulf1 and Sulf2 differentially contribute to the generation of organ-specific sulfation patterns of heparan sulfate.
Sulf-1 and Sulf-2 are essential regulators of GDNF signaling in the SSC niche and direct downstream targets of Sertoli cell-specific transcriptional factor Wilm's tumor 1.
reduction in protein levels promotes satellite cell proliferation
These results reveal that Sulf1 and Sulf2 fulfil non-redundant functions in vivo in the development and maintenance of the murine nervous system.
The data identify sulfatase 1 as an inhibitor of prostatic branching morphogenesis and growth factor signaling that is down-regulated as part of the normal response to androgen action in the male urogenital sinus.
results show that Sulf1 and Sulf2 play overlapping yet critical roles in mouse development and are redundant and essential for neonatal survival
Sulfs are extracellular endosulfatases with strong potential for modulating the interactions of heparan sulfate proteoglycans in the extracellular microenvironment
Sulf2 may have roles in several tissues but that there is compensation by and/or redundancy with Sulf1.
SULF1 is expressed in GDNF-expressing esophageal muscle and SULF2 in innervating neurons, establishing their direct functions in esophageal innervation.
Results establish Sulfs 1 and 2 as essential regulators of heparan sulfate-dependent growth factor signaling in the adult muscle stem cell niche.
Redundant function of the heparan sulfate 6-O-endosulfatases Sulf1 and Sulf2 in fine-tuning rather than regulating the development of skeletal structures.
lack of SULF1 expression downregulates VEGFA-mediated arterial marker expression, confirming that Sulf1 mediates arterial specification by regulating VegfA165 activity.
Sulf1 triggers Shh signaling activity to establish and, later on, modify the spatial arrangement of gene expression in ventral neural progenitors
Data indicate that sulf1 plays a crucial role in modulating both BMP and FGF signaling.
Zebrafish sulf1 and sulf2a are broadly expressed in the central nervous system (CNS) and non-neuronal tissue including heart, somite boundaries, olfactory system, and otic vesicle.
Heparan sulfate proteoglycans (HSPGs) act as coreceptors for numerous heparin-binding growth factors and cytokines and are involved in cell signaling. Heparan sulfate 6-O-endosulfatases, such as SULF1, selectively remove 6-O-sulfate groups from heparan sulfate. This activity modulates the effects of heparan sulfate by altering binding sites for signaling molecules (Dai et al., 2005
extracellular sulfatase Sulf-1
, sulfatase FP
, sulfatase FP1c
, sulfatase 1
, extracellular 6-O-endosulfatase
, extracellular sulfatase Sulf-1-like