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The protein encoded by PPP1R14A belongs to the protein phosphatase 1 (PP1) inhibitor family. Additionally we are shipping Protein Phosphatase 1, Regulatory (Inhibitor) Subunit 14A Antibodies (49) and Protein Phosphatase 1, Regulatory (Inhibitor) Subunit 14A Proteins (13) and many more products for this protein.
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Hoxb1b is likely to directly regulate ppp1r14al expression in rhombomere 4. Furthermore, ppp1r14al is essential for establishment of the earliest hindbrain signaling-center in rhombomere 4 by regulating expression of fgf3 (show FGF3 ELISA Kits).
CPI-17 drives Ras activity and tumorigenesis in melanomas in a two-fold way; inactivation of the tumor suppressor merlin and activation of the growth promoting ERM family.
The authors call the mutual sequestration mechanism through which pCPI-17 and myosin light-chain phosphatase interact inhibition by unfair competition: myosin light-chain phosphatase protects pCPI-17 from other phosphatases, while pCPI-17 blocks other substrates from the active site of myosin light-chain phosphatase.
Study finds that CPI-17 (PPP1R14A protein phosphatase 1 regulatory inhibitor subunit 14A, 17 kDa) is not expressed in the healthy peripheral nervous system or in nontumour pathologies of the peripheral nervous system. CPI-17 up-regulation, however, is observed in over 90% of schwannomas, but not in neurofibroma and only rarely in malignant peripheral nerve sheath tumour.
CPI-17 has a role in restoring skin homoeostasis in cutaneous field of cancerization lesions
analysis of the interaction between plakoglobin (show JUP ELISA Kits) and CPI-17, which is affected by the phosphorylation status of CPI-17 in human lung microvascular endothelial cells
The N-terminal 21-residue tail domain of CPI-17 is necessary for nuclear localization. Phospho-mimetic Asp (show ASIP ELISA Kits)-substitution of CPI-17 at Ser12 attenuates the nuclear import.
The study characterized the CPI-17 promoter and identified binding sites for GATA-6 (show GATA6 ELISA Kits) and nuclear factor kappa B (NF-kappaB (show NFKB1 ELISA Kits)).
a novel signaling cascade that links RhoA (show RHOA ELISA Kits)-mediated calcium sensitivity to MEF2 (show MEF2A ELISA Kits)-dependent myocardin (show MYOCD ELISA Kits) expression in VSMCs through a mechanism involving p38 MAPK (show MAPK14 ELISA Kits), PP1alpha (show PPP1CA ELISA Kits), and CPI-17.
RACK1 (show GNB2L1 ELISA Kits) may play a role in PKC/CPI-17 signaling pathway.
cAMP/PKA regulates the endothelial barrier via inhibition of the contractile machinery, mainly by the activation of MLCP via inhibition of CPI-17 and RhoA (show RHOA ELISA Kits)/Rock.
Enhanced vasorelaxation in early endotoxemia is mediated by redox signaling through PKG-1alpha but in later endotoxemia by myosin phosphatase isoform shifts enhancing sensitivity to NO/cGMP as well as smooth muscle atrophy.
a novel signaling cascade that links RhoA (show RHOA ELISA Kits)-mediated calcium sensitivity to MEF2 (show MEF2C ELISA Kits)-dependent myocardin (show MYOCD ELISA Kits) expression in VSMCs through a mechanism involving p38 MAPK (show MAPK14 ELISA Kits), PP1alpha (show PPP1CA ELISA Kits), and CPI-17.
Data suggest that CPI-17 and both conventional and novel PKC isozymes contribute to the phasic and tonic contractile components of BALB/c colonic circular smooth muscle.
Organ-specific mechanisms involving MYPT1 (show PPP1R12A ELISA Kits), M-RIP, and CPI-17 are critical to regulating basal LC20 (show MYL9 ELISA Kits) phosphorylation in gastrointestinal smooth muscles.
calcium-independent phospholipase A2beta has a role in high glucose-induced activation of RhoA (show RHOA ELISA Kits), Rho kinase (show ROCK2 ELISA Kits), and CPI-17 in cultured vascular smooth muscle cells and vascular smooth muscle hypercontractility in diabetic animals
distribution of mouse and rat PPP1R14A was more specific and different from that of humans
concluded that actions downstream of cGMP/PKG (show PRKG1 ELISA Kits) can reverse PKC (show PKC ELISA Kits)-mediated phosphorylation of CPI-17 and Ca(2 (show CA2 ELISA Kits)+) sensitization in smooth muscle
findings suggest that CPI-17 was downregulated during intestinal inflammation and that TNF-alpha (show TNF ELISA Kits) plays a central role in this process. Downregulation of CPI-17 may play a role in motility impairments in inflammation.
CPI-17 expression is reversibly controlled in response to the phenotype transition of smooth muscle cells that restricts the signal to differentiated smooth muscle cells and particular cell types.
This study examined the protein expression and spatial-temporal distribution of PKCalpha (show PKCa ELISA Kits) and CPI-17 in intact smooth muscle tissues.
The protein encoded by this gene belongs to the protein phosphatase 1 (PP1) inhibitor family. This protein is an inhibitor of smooth muscle myosin phosphatase, and has higher inhibitory activity when phosphorylated. Inhibition of myosin phosphatase leads to increased myosin phosphorylation and enhanced smooth muscle contraction. Alternatively spliced transcript variants encoding different isoforms have been noted for this gene.
protein phosphatase 1, regulatory (inhibitor) subunit 14A
, protein phosphatase 1 regulatory subunit 14A
, 17 kDa PKC-potentiated inhibitory protein of PP1
, 17-KDa protein
, 17-kDa PKC-potentiated inhibitory protein of PP1
, PKC-potentiated inhibitory protein of PP1
, protein kinase C-potentiated inhibitor protein of 17 kDa