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Validated All-in-One™ qPCR Primer for TRPM7(NM_017672.5) Search again
Product ID:
HQP013734
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALSPDC, CHAK, CHAK1, LTRPC7, LTrpC-7, TRP-PLIK
Gene Description:
transient receptor potential cation channel subfamily M member 7
Target Gene Accession:
NM_017672.5(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
TRPCs, mammalian homologs of the Drosophila transient receptor potential (trp) protein, are ion channels that are thought to mediate capacitative calcium entry into the cell. TRP-PLIK is a protein that is both an ion channel and a kinase. As a channel, it conducts calcium and monovalent cations to depolarize cells and increase intracellular calcium. As a kinase, it is capable of phosphorylating itself and other substrates. The kinase activity is necessary for channel function, as shown by its dependence on intracellular ATP and by the kinase mutants.[supplied by OMIM].
Gene References into function
- only Mg(2+) can directly modulate TRPM7/ChaK1 kinase activity in vivo
- TRPM7 activity is up- and down-regulated through its endogenous kinase in a cAMP- and protein kinase A-dependent manner
- TRPM7 is a functionally important regulator of Mg2+ homeostasis and growth in vascular smooth muscle cells.
- A TRPM7 variant shows altered sensitivity to magnesium that may contribute to the pathogenesis of two Guamanian neurodegenerative disorders.
- TRPM7-deficient cells become Mg(2+) deficient & are not viable.TRPM7 is characterized functionally as constitutively active ion channel permeable for variety of cations including Ca & Mg & regulated by intracellular Mg &/or Mg-nucleotide complexes[review
- Although TRPM6 and TRPM7 are closely related and deficiency in either one of these molecules severely affects Mg(2+) homeostasis regulation, TRPM6 and TRPM7 do not appear to be functionally redundant.
- Both endogenous and heterologously expressed TRPM7 was found in tubulovesicular structures that were translocated to the region of the plasma membrane on induction of shear stress.
- Regulation of cell adhesion by TRPM7 is the combined effect of kinase-dependent and -independent pathways on actomyosin contractility.
- the ion channel TRPM7 regulates cell adhesion through m-calpain by mediating the local influx of calcium into peripheral adhesion complexes
- We conclude that the nucleotide-dependent regulation of TRPM7 is mediated by the nucleotide binding site on the channel's endogenous kinase domain and interacts synergistically with a Mg(2+) binding site extrinsic to that domain.
- heterologous expression of TRPM6 but not the mutant TRPM6(S141L) produces functional channels with divalent cation permeability profile and pH sensitivity distinctive from those of TRPM7 channels and TRPM6/7 complexes
- TRPM7 is stretch- and swelling-activated cation channel endogenously expressed in HeLa cells. By serving as swelling-induced Ca(2+) influx pathway, it has important role in cell volume regulation.
- under physiological ionic conditions, TRPM7 currents are activated rather than inhibited by PLC-activating receptor agonists
- the channel may serve as a regulated transport mechanism for these ions that could affect cell adhesion, cell growth and proliferation, and even cell death under pathological stress such as anoxia--{REVIEW}
- We thus conclude that the TRPM7 channel can be directly activated by mechano-stress in a manner independent of exocytosis-mediated incorporation of this channel protein into the plasma membrane.
- TRPM7 senses osmotically induced changes primarily through molecular crowding of solutes that affect channel activity.
- The inner membrane potential (as regulated by proton ionophores) and the F1/FO-ATP synthase of mitochondria are important in regulating TRPM7 channels.
- Human mast cells express functional TRPM7 channels that are a critical requirement for cell survival.
- The subjects who carried >or=1 1482Ile allele and who consumed diets with a high Ca:Mg intake were at a higher risk of adenoma and hyperplastic polyps than were the subjects who did not carry the polymorphism
- Transient receptor potential melastatin 7-like current has a role in cell proliferation in human head and neck carcinoma cells
- restoration of only two "ancient" pore residues in human TRPM2 (Q981E/P983Y) significantly increased (approximately 4-fold) its permeability for Ca(2+).
- This review discusses the importance of magnesium in vascular biology and implications in hypertension and highlights the transport systems, particularly TRPM7--REVIEW
- The predominant Mg transporters include TRPM6 and TRPM7
- findings support a model where massive autophosphorylation outside the catalytic domain of TRPM6 and TRPM7 may facilitate kinase-substrate interactions leading to enhanced phosphorylation of those substrates
- proton conductivity of endogenous human TRPM7 plays a role in physiologically/pathologically acidic situations.
- TRPM6 and TRPM7 phosphorylate the assembly domain of myosin IIA, IIB and IIC on identical residues.
- in human TRPM7, both Asp-1054 and Glu-1052, may provide binding sites for Mg(2+) and Ca(2+); Asp-1054 is an essential determinant of Mg(2+)and Ca(2+) conductivity; Glu-1052 and Asp-1059 facilitate conduction of divalent cations
- Suppression of TRPM7 induces cell death in gastric cancer.
- bradykinin regulates TRPM7 and its downstream target annexin-1 through phospholipase C-dependent, protein kinase C-dependent and c-Src-dependent and cAMP-independent pathways.
- there was no evidence of association between common TRPM7 haplotypes and diabetes risk