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Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer [mRNA]

ABSTRACT: Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer [mRNA]

PROVIDER: PRJNA515879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8454880_1.fastq.gz	Fastqsanger.gz
	SRR8454880_2.fastq.gz	Fastqsanger.gz
	SRR8454872_1.fastq.gz	Fastqsanger.gz
	SRR8454872_2.fastq.gz	Fastqsanger.gz
	SRR8454873_1.fastq.gz	Fastqsanger.gz

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Identification of a novel MYC-TINCR-EGFR signaling pathway loop

Project description:Identification of a novel MYC-TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer through examination of transcription factor C-MYC binding in 2 cell types.

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Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer

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Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer

Project description:RNA sequencing was performed to investigate the potential crosstalk between TINCR and microRNAs.

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Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer [mRNA]

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Profiling uterine fibroid specimens with an in-house array representing all 90 human tyrosine kinases and their ligands

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LKB1 inactivation initiates a chromatin remodeling cascade to drive metastatic progression

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Control of Somatic Tissue Differentiation by the Long Non-Coding RNA TINCR (HTS)

Project description:Several of the thousands of human long non-coding RNAs (lncRNAs) have been functionally characterized; however, potential roles for lncRNAs in somatic tissue differentiation remain poorly understood. Here we show that a 3.7kb lncRNA, terminal differentiation-induced ncRNA (TINCR), controls human epidermal differentiation by a post-transcriptional mechanism. TINCR is required for high mRNA abundance of key differentiation genes, many of which are mutated in human skin diseases, including FLG, LOR, ALOXE3, ALOX12B, ABCA12, CASP14 and ELOVL3. TINCR-deficient epidermis lacked terminal differentiation ultrastructure, including keratohyalin granules and intact lamellar bodies. Genome-scale RNA interactome analysis revealed that TINCR interacts with a suite of differentiation mRNAs. TINCR-mRNA interaction occurs through a 25 nucleotide M-bM-^@M-^\TINCR boxM-bM-^@M-^] motif which is strongly enriched in interacting mRNAs and required for TINCR binding. A high-throughput screen to analyze TINCR binding capacity to ~9,400 human recombinant proteins revealed direct binding of TINCR RNA to the Staufen1 (STAU1) protein. STAU1-deficient tissue recapitulated the impaired differentiation seen with TINCR depletion. Loss of UPF1 and UPF2, both of which are required for STAU1-mediated RNA decay (SMD), however, lacked differentiation impacts. Instead, the TINCR/STAU1 complex seems to mediate stabilization of differentiation mRNAs, such as KRT80. These data identify TINCR as a key lncRNA required for somatic tissue differentiation, which occurs through inducible lncRNA binding to differentiation mRNAs to ensure their expression. Examination of TINCR-binding RNAs using two independent pools of TINCR-targeting oligos

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