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ULK1 Antibody (Center S556)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | O75385 |
| Other Accession | NP_003556.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 112631 Da |
| Antigen Region | 538-564 aa |
| Gene ID | 8408 |
|---|---|
| Other Names | Serine/threonine-protein kinase ULK1, Autophagy-related protein 1 homolog, ATG1, hATG1, Unc-51-like kinase 1, ULK1, KIAA0722 |
| Target/Specificity | This ULK1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 538-564 amino acids from the Central region of human ULK1. |
| Dilution | WB~~1:1000 |
| 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 | ULK1 Antibody (Center S556) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ULK1 {ECO:0000303|PubMed:9693035, ECO:0000312|HGNC:HGNC:12558} |
|---|---|
| Function | Serine/threonine-protein kinase involved in autophagy in response to starvation (PubMed:18936157, PubMed:21460634, PubMed:21795849, PubMed:23524951, PubMed:25040165, PubMed:29487085, PubMed:31123703). Acts upstream of phosphatidylinositol 3-kinase PIK3C3 to regulate the formation of autophagophores, the precursors of autophagosomes (PubMed:18936157, PubMed:21460634, PubMed:21795849, PubMed:25040165). Part of regulatory feedback loops in autophagy: acts both as a downstream effector and negative regulator of mammalian target of rapamycin complex 1 (mTORC1) via interaction with RPTOR (PubMed:21795849). Activated via phosphorylation by AMPK and also acts as a regulator of AMPK by mediating phosphorylation of AMPK subunits PRKAA1, PRKAB2 and PRKAG1, leading to negatively regulate AMPK activity (PubMed:21460634). May phosphorylate ATG13/KIAA0652 and RPTOR; however such data need additional evidences (PubMed:18936157). Plays a role early in neuronal differentiation and is required for granule cell axon formation (PubMed:11146101). Also phosphorylates SESN2 and SQSTM1 to regulate autophagy (PubMed:25040165, PubMed:37306101). Phosphorylates FLCN, promoting autophagy (PubMed:25126726). Phosphorylates AMBRA1 in response to autophagy induction, releasing AMBRA1 from the cytoskeletal docking site to induce autophagosome nucleation (PubMed:20921139). Phosphorylates ATG4B, leading to inhibit autophagy by decreasing both proteolytic activation and delipidation activities of ATG4B (PubMed:28821708). |
| Cellular Location | Cytoplasm, cytosol. Preautophagosomal structure. Note=Under starvation conditions, is localized to puncate structures primarily representing the isolation membrane that sequesters a portion of the cytoplasm resulting in the formation of an autophagosome. |
| Tissue Location | Ubiquitously expressed. Detected in the following adult tissues: skeletal muscle, heart, pancreas, brain, placenta, liver, kidney, and lung |
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Provided below are standard protocols that you may find useful for product applications.
Background
ULK1 is involved in autophagy. Required for autophagosome formation (By similarity). Target of the TOR kinase signaling pathway that regulates autophagy through the control of phosphorylation status of ATG13/KIAA0652 and ULK1, and the regulation of the ATG13-ULK1-RB1CC1 complex (By similarity). Phosphorylates ATG13/KIAA0652. Involved in axon growth (By similarity). Plays an essential role in neurite extension of cerebellar granule cells (By similarity).
References
Mercer, C.A., et al. Autophagy 5(5):649-662(2009)
Ganley, I.G., et al. J. Biol. Chem. 284(18):12297-12305(2009)
Jung, C.H., et al. Mol. Biol. Cell 20(7):1992-2003(2009)
Hosokawa, N., et al. Mol. Biol. Cell 20(7):1981-1991(2009)
Chan, E.Y. Sci Signal 2 (84), PE51 (2009) :
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