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Validated All-in-One™ qPCR Primer for FKBP1A(NM_000801.4) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene is a member of the immunophilin protein family, which play a role in immunoregulation and basic cellular processes involving protein folding and trafficking. The protein is a cis-trans prolyl isomerase that binds the immunosuppressants FK506 and rapamycin. It interacts with several intracellular signal transduction proteins including type I TGF-beta receptor. It also interacts with multiple intracellular calcium release channels, and coordinates multi-protein complex formation of the tetrameric skeletal muscle ryanodine receptor. In mouse, deletion of this homologous gene causes congenital heart disorder known as noncompaction of left ventricular myocardium.
Gene References into function
- It is likely that in FKBP12-ligand complexes, tryptophan 59 provides added binding energy at the active site at the expense of protein stability, a characteristic common to other proteins.
- folding and kinetics of human FKBP12
- the central binding site for the 12 kDa FK506-binding protein of type-3 ryanodine receptor, encompassing the critical valine proline motif, plays a crucial role in the modulation of the Ca2+ release properties
- experimental data on the stability of FKBP12 are reported for the effects of three environmental variables: pH, salt, and macromolecular crowding
- The spinal horn neurons stained with anti-FKBP 12 antibody was significantly decreased in the motor neuron disease cases compared to that in controls.
- FKBP12 accelerated the aggregation of alpha-synuclein in vitro.
- These findings indicate a new inhibitory function of FKBP12 as an adaptor molecule for the Smad7-Smurf1 complex to regulate the duration of the activin signal through activin type I receptors.
- characterization of the stability, binding and enzymatic properties of three FK506 binding proteins (FKBP-12) differing only by the length and sequence of their N-terminus
- Data show that insertion of a chaperone domain from E. coli SlyD converts human FKBP12 into a powerful catalyst of protein folding.
- FKBP12.0-RyR2 interaction can regulate the gain of excitation-contraction coupling in cardiomyocytes
- FKBP12 is predominantly present during early neointima formation, while mature neointimal atheromas show a relatively low expression without confinement to luminal areas.
- fndings suggest that the peptidyl-prolyl isomerase activity requires only the hydrophobic cavity that captures the Pro-containing peptide
- We investigated in detail the effect of FKBP12 on early aggregation and on fibril formation of wild-type, A53T and A30P alpha-SYN. FKBP12 has a much smaller effect on the fibril formation of these two clinical mutants of alpha-SYN.
- CCI-779 inhibits mTOR signaling through an FKBP12-independent mechanism that leads to profound translational repression in cancer cells.