High impact information on FRS3

• In the present report, we show that expression of SNT-2 suppressed EGF-induced cell transformation and proliferation, and expression level of SNT-2 is downregulated in cancer [1].
• Altogether, our data indicate that the FRS2 and FRS3 adapters may have a role in thyroid carcinogenesis triggered by TRK oncogenes [2].
• In addition, RNAi-mediated decrease in ULK2 causes increased interaction between FGFR1 and FRS3 [3].
• In contrast, the mutant SNT-2 which carries deletion of 186-252 amino acids and lacks ERK2 binding does not have these effects [4].
• Both FRS2 and FRS3 contain 5 coding exons spanning over 7 kb of genomic sequence with similar exon sizes and organization [5].

Biological context of FRS3

• Non-coding sequences, highly conserved between mouse and human, were identified in the FRS3 introns that may potentially function as regulatory elements [5].

Associations of FRS3 with chemical compounds

• Luminescent silica nanotubes SNT-2 (loaded with coumarion laser dye 2) and SNT-3 (loaded with anthracene laser dye 3) were prepared by sol-gel cocondensation of functional dyes and TEOS in a cholesterol-based organogel system [6].

Other interactions of FRS3

• Furthermore, SNT-2 constitutively bound to EGFR through the phosphotyrosine binding (PTB) domain both with and without EGF stimulation [1].

Analytical, diagnostic and therapeutic context of FRS3

• To assay potential differences in their patterns of expression, RT-PCR analysis was used to assay FRS2 and FRS3 expression in the developing embryo and neural tube (NT) during the time of neurogenesis [5].
• Comparative genomic sequence analyses show a highly conserved genomic organization between mouse and human in both FRS2 and FRS3 genes [5].

References