Lmna (NM_001002011) Mouse Tagged ORF Clone Lentiviral Particle
CAT#: MR209880L4V
- LentiORF®
-
Lenti ORF particles, Lmna (GFP-tagged) - Mouse lamin A (Lmna), transcript variant 1, 200ul, >10^7 TU/mL
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Specifications
Product Data | |
Type | Mouse Tagged ORF Clone |
Tag | mGFP |
Symbol | Lmna |
Synonyms | Dhe |
Mammalian Cell Selection | Puromycin |
Vector | pLenti-C-mGFP-P2A-Puro |
ACCN | NM_001002011 |
ORF Size | 1995 bp |
Sequence Data |
The ORF insert of this clone is exactly the same as(MR209880).
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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_001002011.3, NP_001002011.2 |
RefSeq Size | 3189 bp |
RefSeq ORF | 1998 bp |
Locus ID | 16905 |
Cytogenetics | 3 38.84 cM |
Gene Summary | This gene encodes a protein that is a member of the lamin family. Nuclear lamins, intermediate filament-like proteins, are the major components of the nuclear lamina, a protein meshwork associated with the inner nuclear membrane. This meshwork is thought to maintain the integrity of the nuclear envelope, participate in chromatin organization, and regulate gene transcription. Vertebrate lamins consist of two types, A and B. This protein is an A-type and is proposed to be developmentally regulated. In mouse deficiency of this gene is associated with muscular dystrophy. Mouse lines with different mutations in this gene serve as pathophysiological models for several human laminopathies. In humans, mutations in this gene lead to several diseases: Emery-Dreifuss muscular dystrophy, familial partial lipodystrophy, limb girdle muscular dystrophy, dilated cardiomyopathy, Charcot-Marie-Tooth disease, and Hutchinson-Gilford progeria syndrome. Alternative splicing results in multiple transcript variants that encode different protein isoforms. [provided by RefSeq, May 2013] |
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