Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 10 bp insertion in exon 3
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-GLYR1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
GLYR1 also known as glyoxylate reductase 1 homolog or NP60 is a 62 kDa protein. It is an NAD(P)H-dependent oxidoreductase and binds specifically to histones modifying their methylation status. GLYR1 shows expression in various tissues with higher levels noted in the kidney and liver. It plays a role in chromatin remodeling indicating its involvement in gene expression regulation.
Biological function summary
GLYR1 influences chromatin structure by regulating histone H3 lysine 36 trimethylation (H3K36me3). It interacts with lysine-specific demethylase 1 (LSD1) and partners within chromatin-modifying complexes. Through these interactions GLYR1 can impact transcriptional repression and activation. Its activity shows specific importance in controlling gene expression related to cell growth and differentiation.
Pathways
GLYR1 interacts with components of the MAPK signaling pathway and the histone modification pathway. It works alongside proteins like LSD1 and histone deacetylases (HDACs) to modulate transcriptional outcomes. These interactions provide evidence of its role in transmitting extracellular signals to the nucleus ultimately influencing gene expression patterns.
Research links GLYR1 to cancer progression and inflammatory responses. Its overexpression or dysregulation has associations with tumors where alteration of histone marks leads to aberrant gene expression. GLYR1 also connects with proteins like HDACs in these diseases contributing to the modulation of cell cycle and apoptosis which are critical for cancer development.
