Phospho-ULK1 (Ser556) Antibody (YA7534)
(Synonyms: KIAA0722, ULK1, Serine/threonine-protein kinase ULK1, Autophagy-related protein 1 homolog, Unc-51-like kinase 1, ATG1, hATG1)
Based on 1 Customer Validation
Phospho-ULK1 (Ser556) Antibody (YA7534) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to Phospho-ULK1 (Ser556).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF, ELISA
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05% BSA.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:2000-1:10000 | 1:200-1:1000 | 1:5000-1:20000 |
Product Details
Phospho-ULK1 (Ser556) Antibody (YA7534) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to Phospho-ULK1 (Ser556).
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 130 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 113 kDa
The exact sequence is proprietary to MCE.
Endogenous
Protein A affinity purified
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05% BSA.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
ULK1 is a serine/threonine kinase and a key initiator of mammalian autophagy, functioning near the apex of a nutrient-sensitive regulatory pathway[1]. Mechanistically, AMPK binds ULK1 and supports ULK1-mediated autophagy, while mTORC1 negatively regulates the ULK1 autophagic complex through phosphorylation-dependent control[2][3]. During starvation, ULK1 links cellular energy sensing to downstream autophagy machinery, including ATG13, FIP200/RB1CC1, ATG101, ATG14L, VPS34, and phagophore formation[3][4]. In disease models, altered ULK1 signaling has been connected with prostate cancer progression, prion infection, clear cell renal cell carcinoma, cardiomyocyte oxidative injury, and pathogen-related autophagy[5][6][7][8][9]. Compared with ULK2, ULK1 shows strong functional overlap in nutrient-starvation autophagy, because combined ULK1/ULK2 loss disrupts autophagy activation more clearly than single loss[10]. Compared with ULK3, ULK1 remains part of the canonical mTOR-AMPK autophagy axis, whereas ULK3 can support mTOR-insensitive autophagic flux in BIN1-deficient hippocampal neurons[11]. For experimental applications, ULK1 pathway modulation can be studied with AMPK activators, mTOR inhibitors, deubiquitinase inhibitor WP1130, and pathway inhibitors targeting CAMKK2-AMPK-ULK1 signaling[2][5][12].
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Subcellular Localization
Cytoplasm, cytosol,Preautophagosomal structure
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Expression
Tissue_Specificity: Ubiquitously expressed. Detected in the following adult tissues: skeletal muscle, heart, pancreas, brain, placenta, liver, kidney, and lung -
Isoforms & Post-Translational Modification
O75385: 1050 amino acids, molecular weight 112631 Da.
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Subunit
Interacts with GABARAP and GABARAPL2 (PubMed:11146101)
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SwissProt ID
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Synonyms
KIAA0722, ULK1, Serine/threonine-protein kinase ULK1, Autophagy-related protein 1 homolog, Unc-51-like kinase 1, ATG1, hATG1
Documentation
References
[1]. Chan EY. Regulation and function of uncoordinated-51 like kinase proteins. Antioxid Redox Signal. 2012 Sep 1;17(5):775-85. doi: 10.1089/ars.2011.4396. Epub 2012 Jan 4. PMID: 22074133. et al. Regulation and function of uncoordinated-51 like kinase proteins. Antioxid Redox Signal. 2012 Sep 1;17(5):775-85. [Content Brief]
[2]. Lee JW, et al. The association of AMPK with ULK1 regulates autophagy. PLoS One. 2010 Nov 3;5(11):e15394. [Content Brief]
[3]. Roach PJ. AMPK -> ULK1 -> autophagy. Mol Cell Biol. 2011 Aug;31(15):3082-4. doi: 10.1128/MCB.05565-11. Epub 2011 May 31. PMID: 21628530; PMCID: PMC3147606. et al. AMPK -> ULK1 -> autophagy. Mol Cell Biol. 2011 Aug;31(15):3082-4. [Content Brief]
[4]. Pyo KE, et al. ULK1 O-GlcNAcylation Is Crucial for Activating VPS34 via ATG14L during Autophagy Initiation. Cell Rep. 2018 Dec 4;25(10):2878-2890.e4. [Content Brief]
[5]. Lin C, et al. Inhibition of CAMKK2 impairs autophagy and castration-resistant prostate cancer via suppression of AMPK-ULK1 signaling. Oncogene. 2021 Mar;40(9):1690-1705. [Content Brief]
[6]. Fan XY, et al. Activation of the AMPK-ULK1 pathway plays an important role in autophagy during prion infection. Sci Rep. 2015 Oct 1;5:14728. [Content Brief]
[7]. Radovanovic M, et al. Role of AMPK/mTOR-independent autophagy in clear cell renal cell carcinoma. J Investig Med. 2020 Dec;68(8):1386-1393. [Content Brief]
[8]. Xie C, et al. A novel danshensu/tetramethypyrazine derivative attenuates oxidative stress-induced autophagy injury via the AMPK-mTOR-Ulk1 signaling pathway in cardiomyocytes. Exp Ther Med. 2021 Feb;21(2):118. [Content Brief]
[9]. Yu Y, et al. Guanylate-Binding protein 2b regulates the AMPK/mTOR/ULK1 signalling pathway to induce autophagy during Mycobacterium bovis infection. Virulence. 2022 Dec;13(1):875-889. [Content Brief]
[10]. McAlpine F, et al. Regulation of nutrient-sensitive autophagy by uncoordinated 51-like kinases 1 and 2. Autophagy. 2013 Mar;9(3):361-73. [Content Brief]
[11]. Jin Y, et al. BIN1 deficiency enhances ULK3-dependent autophagic flux and reduces dendritic size in mouse hippocampal neurons. Autophagy. 2025 Jan;21(1):223-242. [Content Brief]
[12]. Drießen S, et al. Deubiquitinase inhibition by WP1130 leads to ULK1 aggregation and blockade of autophagy. Autophagy. 2015;11(9):1458-70. [Content Brief]
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