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TRIP15 (COPS2) (NM_004236) Human Tagged ORF Clone Lentiviral Particle
CAT＃: RC203159L2V
- LentiORF®
-
Lenti ORF particles, COPS2 (mGFP-tagged) - Human COP9 constitutive photomorphogenic homolog subunit 2 (Arabidopsis) (COPS2), transcript variant 1, 200ul, >10^7 TU/mL
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CNY 9,975.00
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Specifications
| Product Data | |
| Product Name | TRIP15 (COPS2) (NM_004236) Human Tagged ORF Clone Lentiviral Particle |
| Synonyms | ALIEN; CSN2; SGN2; TRIP15 |
| Vector | pLenti-C-mGFP |
| ACCN | NM_004236 |
| ORF Size | 1329 bp |
| Sequence Data |
The ORF insert of this clone is exactly the same as(RC203159).
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| OTI Disclaimer | The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info |
| OTI Annotation | This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. |
| Reference Data | |
| RefSeq | NM_004236.1 |
| RefSeq Size | 4103 bp |
| RefSeq ORF | 1332 bp |
| Locus ID | 9318 |
| Domains | PCI |
| Protein Families | Druggable Genome, Transcription Factors |
| MW | 51.6 kDa |
| Gene Summary | Essential component of the COP9 signalosome complex (CSN), a complex involved in various cellular and developmental processes. The CSN complex is an essential regulator of the ubiquitin (Ubl) conjugation pathway by mediating the deneddylation of the cullin subunits of SCF-type E3 ligase complexes, leading to decrease the Ubl ligase activity of SCF-type complexes such as SCF, CSA or DDB2. The complex is also involved in phosphorylation of p53/TP53, c-jun/JUN, IkappaBalpha/NFKBIA, ITPK1 and IRF8/ICSBP, possibly via its association with CK2 and PKD kinases. CSN-dependent phosphorylation of TP53 and JUN promotes and protects degradation by the Ubl system, respectively. Involved in early stage of neuronal differentiation via its interaction with NIF3L1.[UniProtKB/Swiss-Prot Function] |
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