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anti-Human PIK3C3 Antikörper:
anti-Rat (Rattus) PIK3C3 Antikörper:
anti-Mouse (Murine) PIK3C3 Antikörper:
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Human Polyclonal PIK3C3 Primary Antibody für ICC, IF - ABIN259946
Huang, Hou, Chen, Zhao, Yan, Zhang, Yang, Kogan, Chen: PML-RARα enhances constitutive autophagic activity through inhibiting the Akt/mTOR pathway. in Autophagy 2011
Show all 4 Pubmed References
Human Polyclonal PIK3C3 Primary Antibody für IF (p), IHC (p) - ABIN711686
Wang, Liang, Lau, Du, Guo, Yan, Gan, Yan, Zhao, Gao, Koch, Ma: Restoring diabetes-induced autophagic flux arrest in ischemic/reperfused heart by ADIPOR (adiponectin receptor) activation involves both AMPK-dependent and AMPK-independent signaling. in Autophagy 2017
Vps34 stimulates tumor development mainly through PKC-delta- activation of p62.
Here we show that a putative fifth subunit, nuclear receptor binding factor 2 (NRBF2 (zeige NRBF2 Antikörper)), is a tightly bound component of the class III phosphatidylinositol 3-kinase complex I that profoundly affects its activity and architecture. NRBF2 (zeige NRBF2 Antikörper) is a homodimer and drives the dimerization of the larger PI3KC3-C1 complex, with implications for the higher-order organization of the preautophagosomal structure.
This study reveals NRBF2 (zeige NRBF2 Antikörper) as a critical molecular switch of PtdIns3K and autophagy activation, and its on/off state is precisely controlled by MTORC1 through phosphorylation.
Atg38 and its human ortholog NRBF2 (zeige NRBF2 Antikörper), accessory components of complex I consisting of Vps15-Vps34-Vps30/Atg6 (zeige BECN1 Antikörper)-Atg14 (yeast) and PIK3R4/VPS15-PIK3C3/VPS34-BECN1/Beclin 1 (zeige BECN1 Antikörper)-ATG14 (human), were characterized.
p300 (zeige EP300 Antikörper)-dependent VPS34 acetylation/deacetylation is the physiological key to VPS34 activation, which controls the initiation of canonical autophagy and of non-canonical autophagy in which the upstream kinases of VPS34 can be bypassed.
Low VPS34 expression is associated with cancer.
Arf tumor suppressor as a new transcriptional target of nuclear EGFR and highlight Vps34 as an important regulator of the nuclear EGFR/Arf survival pathway.
Vps34 has a previously unknown role in regulating Rab7 (zeige RAB7B Antikörper) activity and late endosomal trafficking.
High expression of VPS34 promoted GRP78 (zeige HSPA5 Antikörper) transcription by modulating ATF6 (zeige ATF6 Antikörper). VPS34 could enhance GRP78 (zeige HSPA5 Antikörper) protein stability.
These results establish Vps34 as an essential determinant of both short-term and long-term canonical GPCR signaling.
These results suggest that LEPR, MC4R, PIK3C3 and VRTN are useful markers for accurately predicting breeding values in Duroc pigs.
confirmed that the polymorphism in PIK3C3 (C2604T) has the potential to be a genetic marker for production traits in Duroc pigs
In mouse liver, Vps34 inactivation mildly dampens autophagy, limiting substrate availability for mitochondrial respiration and reducing gluconeogenesis.
AP-1 (zeige JUN Antikörper)/sigma1A (zeige AP1S1 Antikörper)-ArfGAP1 (zeige ARFGAP3 Antikörper)-Rabex-5 (zeige RABGEF1 Antikörper) complex formation leads to more endosomal Rabex-5 (zeige RABGEF1 Antikörper) and enhanced, Rab5 (zeige RAB5A Antikörper)(GTP (zeige AK3 Antikörper))-stimulated Vps34 PI3-kinase (zeige PIK3CA Antikörper) activity, which is essential for multivesicular body endosome formation.
dendritic cells from Vps34-deficient mice have a partially activated phenotype, spontaneously produce cytokines, and exhibit enhanced activity of the classic MHC class I and class II antigen-presentation pathways and displayed a defect in the homeostatic maintenance of splenic CD8alpha(+) dendritic cells and in the capacity of these cells to cross-present cell corpse-associated antigens to MHC class I-restricted T cells.
Results demonstrate that Vps34 is essential for proper myelination by Schwann cells. Depletion of PI3P leads to enlarged late endosomal/lysosomal vacuoles and suppressed trafficking in Schwann cells. Suppressed endosomal trafficking likely causes changes in the abundance and post-translational modification of ErbB2 (zeige ERBB2 Antikörper)/3, a signaling defect that may contribute to arrested myelination in Vps34 deficient nerves.
Phosphatidylinositol-3-phosphate is light-regulated, and Vps34 is essential for survival of retinal rod photoreceptor cells.
This study uncovers a dual role for Vps34 as a regulator of platelet production by megakaryocytes and as an unexpected regulator of platelet activation and arterial thrombus formation dynamics.
E. chaffeensis secretes Etf-1 (zeige ETF1 Antikörper) to induce autophagy to repurpose the host cytoplasm and capture nutrients for its growth through RAB5 (zeige RAB5A Antikörper) and class III PtdIns3K, while avoiding autolysosomal killing.
p300 (zeige NOTCH1 Antikörper)-dependent VPS34 acetylation/deacetylation is the physiological key to VPS34 activation, which controls the initiation of canonical autophagy and of non-canonical autophagy in which the upstream kinases of VPS34 can be bypassed.
Vps34 has a previously unknown role in regulating Rab7 (zeige RAB7A Antikörper) activity and late endosomal trafficking.
Catalytic subunit of the PI3K complex that mediates formation of phosphatidylinositol 3-phosphate which plays a key role in initiation and maturation of autophagosomes. Involved in the transport of lysosomal enzyme precursors to lysosomes. Required for the abcission step in cytokinesis (By similarity).
phosphoinositide-3-kinase, class 3
, phosphatidylinositol 3-kinase catalytic subunit type 3
, PI3K type 3
, PI3-kinase type 3
, ptdIns-3-kinase type 3
, phosphoinositide-3-kinase class 3
, catalytic phosphatidylinositol 3-kinase 3
, PtdIns-3-kinase type 3
, phosphatidylinositol 3-kinase p100 subunit
, class 3 phosphoinositide-3-kinase
, PI-3K Vps34p