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The regulation of PKA localization by AKAP1 may be involved in meiotic resumption and oocyte maturation but not in meiotic incompetence of porcine growing oocytes.
Furthermore, we discuss the role of hypoxia in prompting cellular stress and damage, which has been demonstrated to mediate the proteosomal degradation of AKAP121, leading to an increase in reactive oxgyen species production, mitochondrial dysfunction, and ultimately cell death. [review]
Functional characterization revealed an undescribed role for AMPK (show PRKAA1 ELISA Kits)-dependent phosphorylation of AKAP1 in mitochondrial respiration.
AKAP 149-PKA-PDE4A (show PDE4A ELISA Kits) complex localization is related with YTX effect in K-562 cell line
In the case of the beta2AR (show ADRB2 ELISA Kits), this process is facilitated by the presence of A-Kinase Anchoring Proteins (AKAPs) that serve as scaffolding proteins for the L-type calcium channel and the beta2AR (show ADRB2 ELISA Kits) complex.
AKAP1 anchors Star mRNA at the mitochondria, thus stabilizing the translational complex at this organelle, a situation that might affect STAR production and steroidogenesis.
In tumoural lymphocytes, yessotoxin decreases AKAP149 cytosolic expression and increases cAMP levels which leads to cell death.
Shp2 (show PTPN11 ELISA Kits) is a component of the AKAP-Lbc (show AKAP13 ELISA Kits) complex and is inhibited by protein kinase A under pathological hypertrophic conditions in the heart.
AMY-1 interacts with this and AKAP95 (show AKAP8 ELISA Kits) in the cytoplasm and the nucleus, respectively, and inhibits cAMP-dependent protein kinase (show CDK7 ELISA Kits) activity by preventing binding of its catalytic subunit to A-kinase-anchoring protein (show AKAP13 ELISA Kits) (AKAP) complex.
RIalpha (show PRKAR1A ELISA Kits) and RIbeta (show PRKAR1B ELISA Kits) homodimers as well as an RIalpha:RIbeta heterodimer and several of the mutants were able to bind to the R-binding domain of AKAP149/D-AKAP1
AKAP149-regulated PP1 activity at the NE during G1 is required to maintain nuclear integrity and cell survival.
Genetic ablation of AKAP7 (show AKAP7 ELISA Kits) specifically from dentate granule cells results in disruption of mossy fiber-CA3 (show CA3 ELISA Kits) pyramidal neuron long-term potentiation directly initiated by cAMP, and the AKAP7 (show AKAP7 ELISA Kits) mutant mice are selectively deficient in pattern separation behaviors. The results suggest that the AKAP7 (show AKAP7 ELISA Kits)/PKA complex in the mossy fiber projections plays an essential role in synaptic plasticity and contextual memory formation.
The results demonstrate that Akap1 deficiency promotes cardiac mitochondrial aberrations and mitophagy, enhancing infarct size, pathological cardiac remodeling and mortality under ischemic conditions.
The tongue epithelium is differentiated into multiple epithelial cell layers via the PI3K and PKA pathways in tissue-specific manner during the epithelial-mesenchymal interactions.
Data suggest that D-AKAP1 is a transmembrane protein in mitochondrial outer membrane; D-AKAP1 appears to participate in cAMP signaling; hydrophobicity of D-AKAP1 transmembrane domain regulates localization to either ER or mitochondria.
db/db (show LEPR ELISA Kits)/ mice
NCX3 (show SLC8A3 ELISA Kits) regulates mitochondrial calcium handling from the outer mitochondrial membrane through an AKAP121-anchored signaling complex.
PKC and PKA regulate AChR dynamics at the neuromuscular junction of living mice.
Activation of NOD1 (show NOD1 ELISA Kits) induces lipolysis through NF-kappaB (show NFKB1 ELISA Kits) and the lipolytic PKA activation in 3T3-L1 adipocytes.
hypoxia induces fission of mitochondrial membranes, dependent on availability of protein AKAP121
Six putative caspase (show CASP3 ELISA Kits) substrates, including five novel proteins (ABCF1 (show ABCF1 ELISA Kits), AKAP1, CPE (show CPE ELISA Kits), DOPEY1 and GOPC1 (show GOPC ELISA Kits)) that may be targeted specifically by the initiator caspases 8 and 10 during the early stages of apoptosis, were identified.[caspase 10 (show CASP10 ELISA Kits)]
The A-kinase anchor proteins (AKAPs) are a group of structurally diverse proteins, which have the common function of binding to the regulatory subunit of protein kinase A (PKA) and confining the holoenzyme to discrete locations within the cell. This gene encodes a member of the AKAP family. The encoded protein binds to type I and type II regulatory subunits of PKA and anchors them to the mitochondrion. This protein is speculated to be involved in the cAMP-dependent signal transduction pathway and in directing RNA to a specific cellular compartment.
A kinase (PRKA) anchor protein 1
, A-kinase anchor protein 1
, A kinase anchor protein 1, mitochondrial
, a kinase anchor protein 1, mitochondrial-like
, a-kinase anchor protein 1, mitochondrial-like
, A-kinase anchor protein 1, mitochondrial
, A-kinase anchor protein 149 kDa
, AKAP 149
, dual-specificity A-kinase anchoring protein 1
, protein kinase A anchoring protein 1
, protein kinase A1
, protein phosphatase 1, regulatory subunit 43
, spermatid A-kinase anchor protein 84
, tudor domain containing 17
, a kinase anchor protein 1, mitochondrial
, dual specificity A-kinase-anchoring protein 1
, protein kinase A-anchoring protein 1
, spermatid A-kinase anchor protein
, A-kinase anchor protein 121 kDa
, AKAP 121