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Home MicroRNA 3' UTR Clones

FIP1L1 (NM_001134937) 3β-UTR clone in pMirTarget

| Specifications |
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| Cat. No. |
Description |
Price |
Availability |
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| SC206579 |
3`UTR clone of FIP1 like 1 (S. cerevisiae) (FIP1L1) transcript variant 2 for miRNA target validation |
$495.00 |
4 weeks * |
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* Delivery time is an estimate in business days. Occasional delays may occur due to unforeseen complexities in the preparation of your construct. International customers may expect an additional 1-2 weeks in shipping
Also for FIP1L1 (NM_001134937)
OriGene TrueClone Data
| Vector: | pMirTarget |
Insert Size: 494 |
Restriction Site: SgfI-MluI |
| Sequence Data: | Insert Sequence |
| OTI Disclaimer: | Our molecular clone sequence data has been matched to the sequence identifier above as a point of reference. Note that the complete sequence of this clone is largely the same as the reference sequence but may contain minor differences , e.g., single nucleotide polymorphisms (SNPs). |
| Product Components: | The cDNA clone is shipped in a 2-D bar-coded Matrix tube as 10 ug dried plasmid DNA. The package also includes 100 pmols of both the corresponding 5' and 3' vector primers in separate vials. |
Reference Data
| RefSeq: | NM_001134937.1 |
| Synonyms : | hFip1; Rhe |
| Locus ID: | 81608 |
| Summary: | This gene encodes a subunit of the CPSF (cleavage and polyadenylation specificity factor) complex that polyadenylates the 3' end of mRNA precursors. This gene, the homolog of yeast Fip1 (factor interacting with PAP), binds to U-rich sequences of pre-mRNA and stimulates poly(A) polymerase activity. Its N-terminus contains a PAP-binding site and its C-terminus an RNA-binding domain. An interstitial chromosomal deletion on 4q12 creates an in-frame fusion of human genes FIP1L1 and PDGFRA (platelet-derived growth factor receptor, alpha). The FIP1L1-PDGFRA fusion gene encodes a constitutively activated tyrosine kinase that joins the first 233 amino acids of FIP1L1 to the last 523 amino acids of PDGFRA. This gene fusion and chromosomal deletion is the cause of some forms of idiopathic hypereosinophilic syndrome (HES). This syndrome, recently reclassified as chronic eosinophilic leukemia (CEL), is responsive to treatment with tyrosine kinase inhibitors. Alternative splicing results in multiple transcript variants encoding distinct isoforms. [provided by RefSeq, Oct 2008]. |
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