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Validated All-in-One™ qPCR Primer for PRKAB1(NM_006253.4) Search again
Product ID:
HQP014547
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AMPK, HAMPKb
Gene Description:
protein kinase AMP-activated non-catalytic subunit beta 1
Target Gene Accession:
NM_006253.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By 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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| A | B |
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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 regulatory subunit of the AMP-activated protein kinase (AMPK). AMPK is a heterotrimer consisting of an alpha catalytic subunit, and non-catalytic beta and gamma subunits. AMPK is an important energy-sensing enzyme that monitors cellular energy status. In response to cellular metabolic stresses, AMPK is activated, and thus phosphorylates and inactivates acetyl-CoA carboxylase (ACC) and beta-hydroxy beta-methylglutaryl-CoA reductase (HMGCR), key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. This subunit may be a positive regulator of AMPK activity. The myristoylation and phosphorylation of this subunit have been shown to affect the enzyme activity and cellular localization of AMPK.
Gene References into function
- Dipyridamole, an adenosine transporter inhibitor, and 5'-amino-5'-deoxyadenosine, an adenosine kinase inhibitor, blocked the effect of AICAR on the down-regulation of the insulin receptor protein, mRNA, and promoter activity.
- Reduced activation of AMPK by globular adiponectin in obese and obese type 2 diabetic subjects is not caused by reduced adiponectin receptor expression.
- it is likely that the AMPK-GDE association is a novel mechanism regulating AMPK activity and the resultant fatty acid oxidation and glucose uptake
- These results suggested that the combination of 5-FU and genistein exert a novel chemotherapeutic effect in colon cancers, and AMPK may be a regulatory molecule of COX-2 expression, further implying its involvement in cytotoxicity caused by genistein.
- These are the first data to show an effect of AMPK on cell movement, and suggest a fundamental role for energy deficiency in regulating cellular behaviour.
- These results show that AICAR and insulin/IGF-1 regulate VEGF expression through different mechanisms.
- In conclusion, during prolonged submaximal exercise at 60% VO2peak, higher fat oxidation in women cannot be explained by higher AMPK signalling.
- AMPK phosphorylated TRIP6 in vitro at the N-terminus and the transcriptional co-activator properties of TRIP6 were enhanced by AMPK action.
- AMPK activation and a reduced phosphorylation of 4E-BP1 may contribute to the inhibition of muscle protein synthesis during resistance exercise.
- Endothelial cells possess two pathways to activate AMPK, one Ca2+/CaMKKbeta dependent and one AMP/LKB1 dependent.
- AMPK has a role in regulating growth of cultured human keratinocytes
- modulation of AMPK activity did not affect PI3K/AKT signalling, an advantage for the potential use of AMPK as a target for cancer therapy in LKB1 wild-type tumours
- analysis of a new model for AMPK heterotrimer structure where through its C terminus the beta-subunit binds to the alpha-subunit that, in turn, binds to the gamma-subunit
- Results suggest that FLCN, mutated in Birt-Hogg-Dube syndrome, and its interacting partner FNIP1 may be involved in energy and/or nutrient sensing through the AMPK and mTOR signaling pathways.
- These findings suggest that the activation of JAK2, but not STAT3, may play a critical role in leptin-induced AMPK activation in Huh7 cells.
- AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation.
- phosphatidylinositol 3-kinase/Akt signaling and induces apoptosis is inhibited by energy depletion via AMP-activated protein kinase-dependent phosphorylation of IRS-1 at Ser-794
- 5-Aminoimidazole-4-carboxamide riboside sensitizes TRAIL- and TNF{alpha}-induced cytotoxicity in colon cancer cells through AMP-activated protein kinase signaling
- These results suggest that activation of AMPK inhibits multiple myeloma (MM) cell growth despite stimulation with IL-6, IGF-1, or HS-5 stromal cell conditioned medium and represents a potential new target in the therapy of MM.
- regulation of FOXO3 by AMPK may play a crucial role in fine tuning gene expression programs that control energy balance and stress resistance in cells throughout life
- Grb2 functions as a factor which mediates phosphorylation of AMPK at Thr172.
- AMPK activated by fluid shear stress is a novel regulator of FoxO1a phosphorylation and protein levels.
- metformin-mediated AMPK activation leads to inhibition of mTOR and a reduction in translation initiation
- findings show that that a beta1(186-270)gamma1 complex can form in the absence of detectable alpha subunit and that beta1 Thr-263 and Tyr-267 are required for betagamma association but not alphabeta association
- Inhibition of SIRT1 in telomerase-immortalized human cells and hematopoietic stem cells obtained from SIRT1-deficient mice enhanced cell growth under normal and nutrient limiting conditions.
- AMP-activated protein kinase (AMPK) regulates GLUT4 transcription through the histone deacetylase (HDAC)5 transcriptional repressor.
- the activities of AMP-activated protein kinase, protein kinase B, and mammalian target of rapamycin by limiting energy availability with 2-deoxyglucose
- AMPK inhibits TGFbeta-induced transcription downstream of Smad3 COOH-terminal phosphorylation and nuclear translocation
- AMPK activity is a key determinant of HIF-1 functions in response to reactive oxygen species and may be involffed in HIF-1 regulatory mechanisms.
- AMPK regulates the proteasomal activity under conditions of energy demand.
- modulating basal AMPK and CAMKKB activity in the hypothalamus is essential for maintaining tight regulation of pathways contributing to food intake
- UVB irradfiation regulates COX2 mRNA stability through AMPK and HuR in human keratinocytes.
- Results report that oxygen deprivation can activate the autophagic pathway in human cancer cell lines via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L.
- Data suggest that increased expression of malonyl CoA decarboxylase, and the decreased expression of acetyl CoA carboxylase and 5'-AMP activated protein kinase are important regulators of the maturation of fatty acid oxidation in the newborn human heart.
- Akt and AMPK have roles in the pathway of hydrogen peroxide-activated endothelial nitric-oxide synthase phosphorylation and function
- AMP-activated protein kinase contributes to UV- and H2O2-induced apoptosis in human skin keratinocytes
- The proliferation potential of senescent human diploid fibroblasts can be modulated through the regulation of the AMPK signaling pathway.
- These findings raise the possibility that glucose-induced changes in AMPK are linked to alterations in SIRT1 abundance and activity and possibly cellular redox state.