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PHLDA3 (NM_012396) Human Tagged ORF Clone Lentiviral Particle

  • LentiORF®
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SKU
RC206751L1V
Lenti ORF particles, PHLDA3 (Myc-DDK tagged) - Human pleckstrin homology-like domain, family A, member 3 (PHLDA3), 200ul, >10^7 TU/mL
  $700.00
5 Weeks*
Bulk Requests & Clone Modifications

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Other products for "PHLDA3 or NM_012396"

Specifications
Specifications
Product Data
Type Human Tagged ORF Clone Lentiviral Particle
Tag Myc-DDK
Target Symbol PHLDA3
Synonyms TIH1
Vector pLenti-C-Myc-DDK
Mammalian Cell Selection None
Sequence Data
ORF Nucleotide Sequence
The ORF insert of this clone is exactly the same as(RC206751).
ACCN NM_012396
ORF Size 381 bp
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.
Shipping Dry Ice
Reference Data
RefSeq NM_012396.2
RefSeq Size 1516 bp
RefSeq ORF 384 bp
Locus ID 23612
UniProt ID Q9Y5J5
Cytogenetics 1q32.1
Domains PH
MW 13.9 kDa
Summary p53/TP53-regulated repressor of Akt/AKT1 signaling. Represses AKT1 by preventing AKT1-binding to membrane lipids, thereby inhibiting AKT1 translocation to the cellular membrane and activation. Contributes to p53/TP53-dependent apoptosis by repressing AKT1 activity. Its direct transcription regulation by p53/TP53 may explain how p53/TP53 can negatively regulate AKT1. May act as a tumor suppressor.UniProtKB/Swiss-Prot Function
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*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen complexities in the preparation of your product. International customers may expect an additional 1-2 weeks in shipping.

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