Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
SUMF1 encodes an enzyme that catalyzes the hydrolysis of sulfate esters by oxidizing a cysteine residue in the substrate sulfatase to an active site 3-oxoalanine residue, which is also known as C-alpha-formylglycine. Additionally we are shipping SUMF1 Proteins (13) and SUMF1 Kits (11) and many more products for this protein.
Showing 10 out of 64 products:
Human Polyclonal SUMF1 Primary Antibody for ELISA, WB - ABIN4356737
Oshikawa, Usami, Kato: Characterization of the arylsulfatase I (ARSI) gene preferentially expressed in the human retinal pigment epithelium cell line ARPE-19. in Molecular vision 2009
We show that SUMF1 expression is affected in COPD (show ARCN1 Antibodies) patients compared to controls, and that SNPs in SUMF1 are associated with an increased risk of COPD (show ARCN1 Antibodies). Certain COPD (show ARCN1 Antibodies)-associated SNPs have effects on either SUMF1 gene expression or on lung function. Collectively, this study shows that SUMF1 is associated with an increased risk of developing COPD (show ARCN1 Antibodies).
SUMF1 catalyses a monooxygenase type of reaction.
This detailed clinical description and follow-up of a cohort of patients, together with the molecular characterisation of their underlying defects, contribute to improved knowledge of multiple sulfatase (show ARSH Antibodies) deficiency.
MSD (show MESDC2 Antibodies) presenting in the newborn period with hypotonia, apnoea, cyanosis and rolling eyes, hepato-splenomegaly and deafness. This patient was compound heterozygous for two so far undescribed SUMF1 mutations (c.191C > A; p.S64X and c.818A > G; p.D273G
The complete kinetic parameters for both forms of FGE are described, along with a proposed mechanism for FGE catalysis that accounts for the copper-dependent activity.
A novel missense mutation & an insertional truncating mutation in SUMF1 gene causing nultiple sulphatase deficiency.
furin (show FURIN Antibodies)-mediated processing of FGE during secretion is a physiological means of higher eukaryotic cells to regulate FGE activity upon exit from the endoplasmic reticulum
Phenotypic outcome in Multiple Sulfatase (show ARSH Antibodies) Deficiency depends on both residual FGE activity as well as protein stability.
This study identified genetic variation of SUMF1 in genes associated with in vivo glutamate (show GRIN1 Antibodies) measured using 1H magnetic resonance spectroscopic imaging in the grey matter of patients with multiple sclerosis.
mutational analysis of SUMF1 in 20 Multiple sulfatase (show ARSH Antibodies) deficiency patients of different ethnic origin
Sumf1(-/-) astrocytes failed to support the survival and function of wild-type cortical neurons, suggesting a non-cell autonomous mechanism for neurodegeneration.
Sumf1 controls hematopoietic stem progenitor cell differentiation and hematopoietic lineage development through FGF and Wnt (show WNT2 Antibodies) signaling.
Sumf1 is indispensable for sulfatase (show ARSH Antibodies) activation in mice and mammals, differently from bacteria, have a single sulfatase (show ARSH Antibodies) modification system
This gene encodes an enzyme that catalyzes the hydrolysis of sulfate esters by oxidizing a cysteine residue in the substrate sulfatase to an active site 3-oxoalanine residue, which is also known as C-alpha-formylglycine. Mutations in this gene cause multiple sulfatase deficiency, a lysosomal storage disorder. Alternative splicing results in multiple transcript variants.
C-alpha-formylglycine-generating enzyme 1
, FGly-generating enzyme
, sulfatase-modifying factor 1
, sulfatase-modifying factor