PI3KC3 Antibody (S34)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 2
- PROTOCOLS
- BACKGROUND
Application
| IHC-P, WB, IF, E |
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Primary Accession | Q8NEB9 |
Other Accession | Q6AZN6, O88763, Q5D891, Q6PF93 |
Reactivity | Human |
Predicted | Mouse, Pig, Rat, Xenopus |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 101549 Da |
Antigen Region | 14-39 aa |
Gene ID | 5289 |
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Other Names | Phosphatidylinositol 3-kinase catalytic subunit type 3, PI3-kinase type 3, PI3K type 3, PtdIns-3-kinase type 3, Phosphatidylinositol 3-kinase p100 subunit, Phosphoinositide-3-kinase class 3, hVps34, PIK3C3, VPS34 |
Target/Specificity | This PI3KC3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 14-39 amino acids from human PI3KC3. |
Dilution | IF~~1:200 WB~~1:1000 IHC-P~~1:100 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | PI3KC3 Antibody (S34) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | PIK3C3 (HGNC:8974) |
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Synonyms | VPS34 {ECO:0000305} |
Function | Catalytic subunit of the PI3K complex that mediates formation of phosphatidylinositol 3-phosphate; different complex forms are believed to play a role in multiple membrane trafficking pathways: PI3KC3-C1 is involved in initiation of autophagosomes and PI3KC3-C2 in maturation of autophagosomes and endocytosis (PubMed:14617358, PubMed:33637724, PubMed:7628435). As part of PI3KC3-C1, promotes endoplasmic reticulum membrane curvature formation prior to vesicle budding (PubMed:32690950). Involved in regulation of degradative endocytic trafficking and required for the abscission step in cytokinesis, probably in the context of PI3KC3-C2 (PubMed:20208530, PubMed:20643123). Involved in the transport of lysosomal enzyme precursors to lysosomes (By similarity). Required for transport from early to late endosomes (By similarity). |
Cellular Location | Midbody. Late endosome. Cytoplasmic vesicle, autophagosome. Note=As component of the PI3K complex I localized to pre-autophagosome structures. As component of the PI3K complex II localized predominantly to endosomes (PubMed:14617358). Localizes also to discrete punctae along the ciliary axoneme and to the base of the ciliary axoneme (By similarity) {ECO:0000250|UniProtKB:Q6PF93, ECO:0000305|PubMed:14617358} |
Tissue Location | Ubiquitously expressed, with a highest expression in skeletal muscle. |
Provided below are standard protocols that you may find useful for product applications.
Background
PI3KC3 is a catalytic subunit of the PI3K complex involved in the transport of lysosomal enzyme precursors to lysosomes. This enzyme acts catalytically to convert 1-phosphatidyl-1D-myo-inositol to 1-phosphatidyl-1D-myo-inositol 3-phosphate. Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). The regulation of the Beclin 1-PI3KC3 complex lipid kinase activity is a critical element in the autophagy signaling pathway.
References
References for protein:
1.Vergne, I., et al., J. Exp. Med. 198(4):653-659 (2003).
2.Volinia, S., et al., EMBO J. 14(14):3339-3348 (1995).
References for U251 cell line:
1. Westermark B.; Pontén J.; Hugosson R. (1973).” Determinants for the establishment of permanent tissue culture lines from human gliomas”. Acta Pathol Microbiol Scand A. 81:791-805. [PMID: 4359449].
2. Pontén, J.,Westermark B. (1978).” Properties of Human Malignant Glioma Cells in Vitro”. Medical Biology 56: 184-193.[PMID: 359950].
3. Geng Y.;Kohli L.; Klocke B.J.; Roth K.A.(2010). “Chloroquine-induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent”. Neuro Oncol. 12(5): 473–481.[ PMID: 20406898].
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