SASH1 antibody
- Known as:
- SASH1 (anti-)
- Catalog number:
- orb101867
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SASH1 antibody
Related genes to: SASH1 antibody
- Gene:
- SASH1 NIH gene
- Name:
- SAM and SH3 domain containing 1
- Previous symbol:
- -
- Synonyms:
- KIAA0790, dJ323M4.1, SH3D6A
- Chromosome:
- 6q24.3-q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-27
- Date modifiied:
- 2018-02-13
Related products to: SASH1 antibody
Related articles to: SASH1 antibody
- Meningiomas are the most common intracranial tumors. DNA methylation analysis in benign and aggressive meningiomas showed decreased methylation and overexpression of hsa-miR-21-5p in atypical and anaplastic tumors. Transcriptomic analysis of distinct WHO grade meningiomas showed multiple predicted hsa-miR-21-5p target genes as differentially expressed. They were mainly related to processes of intercellular and intracellular signaling. Intercellular communication in meningioma was investigated using the deposited scRNA-seq dataset and deconvolution of our RNA-seq data. We found WHO grade-related differences in the microenvironment including inverse correlation between the count of border-associated macrophages (BAM) and the level of hsa-miR-21-5p. Single-cell transcriptomics suggests the role of interleukin 6 in direct communication between tumor cells and BAMs. and are predicted targets of hsa-miR-21-5p downregulated in atypical/anaplastic meningiomas. IL6R downregulation was also confirmed by immunohistochemistry. Hsa-miR-21-5p enhanced proliferation and viability of KT21-MG1 meningioma cells and showed a regulatory effect on , and other predicted target genes , , , and by interacting with 3'UTRs. DNA hypomethylation-related overexpression of hsa-miR-21-5p contributes to aggressive meningioma growth by interaction with multiple target genes, and probably affects microenvironment communication between meningioma cells and BAMs by lowering the IL6R level in tumor tissue. - Source: PubMed
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