SUMF1 Over-expression Lysate Product
- Known as:
- SUMF1 Over-expression Lysate Product
- Catalog number:
- GWB-53A1D8
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- SUMF1 Over-expression Lysate Product
Related genes to: SUMF1 Over-expression Lysate Product
- Gene:
- SUMF1 NIH gene
- Name:
- sulfatase modifying factor 1
- Previous symbol:
- -
- Synonyms:
- FGE, UNQ3037
- Chromosome:
- 3p26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-30
- Date modifiied:
- 2014-11-18
Related products to: SUMF1 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: SUMF1 Over-expression Lysate Product
- Gene therapy for neurological disorders is a rapidly evolving field with many preclinical studies and some successful clinical trials. Selectivity of cell specific targeting, efficiency and safety of administration route, and vector dosing are some of the most challenging aspects that need to be addressed for a successful treatment approach. In clinical practice, intravenous delivery is the most commonly used route of administration of viral vectors but adverse events led to the development of intrathecal delivery as a safer delivery method. Preclinical studies confirm the efficacy of intrathecally injected viral vectors for targeting both the central and peripheral nervous system at lower doses than those systemically-administered, limiting toxicity. Clinical applications of intrathecal gene therapy confirm efficacy and safety in patients. Further preclinical studies are needed to improve current vector capsid and payload technologies, while insights from ongoing clinical trials help to optimise patient selection and immunosuppressive protocols. - Source: PubMed
Publication date: 2026/05/14
Kagiava AlexiaChen XinFinkel Richard SGray Steven JKleopa Kleopas A - The biogenesis of secretory proteins proceeds under sequential quality control checkpoints operating along the exocytic pathway. Unlike other chaperones that reside primarily in the endoplasmic reticulum, ERp44 cycles through the Golgi to control the assembly of polymeric proteins and the localization of a few endoplasmic reticulum resident enzymes (ERAP1, Prx4, Ero1α, and SUMF1). To gain information about its pathophysiological role, we generated ERp44-deficient models. ERp44 KO mice are smaller than control siblings, and show skeletal malformations and delayed bone development, with reduced collagen deposition. Similar skeletal defects were also observed in ERp44 knocked down zebrafish embryos, supporting a conserved role for ERp44 in skeletal development. In cellular models, ERp44 downregulation dramatically affects collagen type 1 deposition, causing intracellular procollagen 1 accumulation. We thus conclude that the levels of ERp44 are crucial for efficient collagen deposition. - Source: PubMed
Publication date: 2026/04/16
Pannese MariaCanciani BarbaraCarnovali MartaDalla Torre MarcoGallucci GianpieroMangiavini LauraMariotti MassimoPanina-Bordignon PaolaVan't Hof RobSitia RobertoAnelli Tiziana - A patient with multiple sulfatase deficiency (MSD) was identified through a lysosomal storage disorder enzyme analysis panel, based on a characteristic pattern of reduced activities across multiple sulfatases. Newborn screening laboratories implement various quality control protocols to assess the integrity of received samples. The quality control policy for identifying heat-denatured samples evaluates several enzyme activity levels to determine if a sample has been compromised by excessive heat. A new quality control policy has been established to differentiate heat-denatured samples from those affected by Multiple Sulfatase Deficiency. - Source: PubMed
Publication date: 2026/01/06
Donti Taraka RDiPerna James CHegde Madhuri R - Oxidative stress (OS) plays a role in hypertension development, but the underlying genetic mechanisms are not completely understood. This study aimed to investigate the association between OS-related genes and hypertension by performing an integrative multi-omics analysis using summary-data-based Mendelian randomization (SMR) and colocalization approaches. - Source: PubMed
Publication date: 2026/03/25
Zhang YueMeng JinyangYan YuchengTang HongZhong DonglingLi YuxiXue PeiwenZhang AnrenJin RongjiangLi Juan - Convergence and extension (C&E) cell movements that elongate the primary embryonic axis are precisely timed during vertebrate gastrulation, but mechanisms controlling their onset remain unknown. Using zebrafish embryonic explants that recapitulate C&E and its timing, we identified sulfatase modifying factor 2 (sumf2) as a candidate trigger gene for C&E onset. sumf2 and its paralog sumf1 encode negative and positive sulfatase regulators, respectively, whose expression levels invert and increase heparan sulfate sulfation during gastrulation. Overexpressing sumf1 or sumf2 causes delayed or precocious C&E, respectively, whereas their loss shifts C&E timing in the opposite direction. We identified Sulf1, a modifier of heparan sulfate proteoglycans (HSPGs), as their key downstream effector and found that altering heparan sulfate sulfation levels shifts C&E onset and suppresses sumf1 and sumf2 mutant phenotypes. This work supports a model in which sumf2 expression reduces sulfatase activity, rewriting HSPG sulfation patterns to promote the onset of C&E morphogenesis. - Source: PubMed
Publication date: 2026/03/31
Cervino Ailen SoledadBasu AmritaWeiss Ryan JKaur Bajwa GursimranMarín-Juez RubénGrimm Sandra LCoarfa CristianWilliams Margot Kossmann