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Crkl (NM_007764) Mouse Tagged ORF Clone Lentiviral Particle
CAT＃: MR225132L4V
- LentiORF®
-
Lenti ORF particles, Crkl (GFP-tagged) - Mouse v-crk sarcoma virus CT10 oncogene homolog (avian)-like (Crkl), 200ul, >10^7 TU/mL
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CNY 8,360.00
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Specifications
| Product Data | |
| Product Name | Crkl (NM_007764) Mouse Tagged ORF Clone Lentiviral Particle |
| Synonyms | 1110025F07Rik; AA589403; AI325100; Cr; Crkol; snoop |
| Vector | pLenti-C-mGFP-P2A-Puro |
| ACCN | NM_007764 |
| ORF Size | 912 bp |
| Sequence Data |
The ORF insert of this clone is exactly the same as(MR225132).
|
| 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_007764.4, NP_031790.2 |
| RefSeq Size | 5050 bp |
| RefSeq ORF | 912 bp |
| Locus ID | 12929 |
| Gene Summary | This gene is part of a family of adapter proteins that mediate formation of signal transduction complexes in response to extracellular stimuli, such as growth and differentiation factors. Protein-protein interactions occur through the SH2 domain, which binds phosphorylated tyrosine residues, and the SH3 domain, which binds proline-rich peptide motifs. These interactions promote recruitment and activation of effector proteins to regulate cell migration, adhesion, and proliferation. In certain mouse genetic backgrounds this protein is essential for embryonic development. It is important for neural crest cell differentiation and survival and is proposed to play an important role in transducing the oncogenic signal of Bcr/Abl. Deletion of this gene in mouse mimics the phenotype of DiGeorge/velocardiofacial syndrome in human. Alternative splicing results in multiple transcript variants that encode different protein isoforms. [provided by RefSeq, Mar 2013] |
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