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AB133766

Anti-ULK1 (phospho S638) antibody [EPR6155]

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(4 Publications)

Rabbit Recombinant Monoclonal ULK1 phospho S638 antibody. Suitable for WB and reacts with Human samples. Cited in 4 publications.

View Alternative Names

KIAA0722, ULK1, Serine/threonine-protein kinase ULK1, Autophagy-related protein 1 homolog, Unc-51-like kinase 1, ATG1, hATG1

2 Images
Western blot - Anti-ULK1 (phospho S638) antibody [EPR6155] (AB133766)
  • WB

Unknown

Western blot - Anti-ULK1 (phospho S638) antibody [EPR6155] (AB133766)

All lanes:

Western blot - Anti-ULK1 (phospho S638) antibody [EPR6155] (ab133766) at 1/1000 dilution

Lane 1:

ULK1 transfected 293T cell lysate at 10 µg

Lane 2:

ULK1 transfected 293T cell lysate, treated with Lambda Phosphatase at 10 µg

Secondary

All lanes:

HRP labelled Goat anti Rabbit IgG at 1/2000 dilution

Predicted band size: 112 kDa

false

OI-RD Scanning - Anti-ULK1 (phospho S638) antibody [EPR6155] (AB133766)
  • OI-RD Scanning

Unknown

OI-RD Scanning - Anti-ULK1 (phospho S638) antibody [EPR6155] (AB133766)

We have systematically measured KD (the equilibrium dissociation constant between the antibody and its antigen), of more than 840 recombinant antibodies to assess not only their individual KD values but also to see the average affinity of antibody. Based on the comparison with published literature values for mouse monoclonal antibodies, Recombinant antibodies appear to be on average 1-2 order of magnitude higher affinity.

  • Carrier free

    Anti-ULK1 (phospho S638) antibody [EPR6155] - BSA and Azide free

Key facts

Host species

Rabbit

Clonality

Monoclonal

Clone number

EPR6155

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

WB

applications

Immunogen

The exact immunogen used to generate this antibody is proprietary information.

Reactivity data

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Product details

Species reactivity
Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species.
Please contact us for more information.

Patented technology
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.

What are the advantages of a recombinant monoclonal antibody?
This product is a recombinant monoclonal antibody, which offers several advantages including:

  • - High batch-to-batch consistency and reproducibility
  • - Improved sensitivity and specificity
  • - Long-term security of supply
  • - Animal-free batch production

For more information, read more on recombinant antibodies.

Properties and storage information

Form
Liquid
Purity
Tissue culture supernatant
Storage buffer
pH: 7.2 - 7.4 Preservative: 0.01% Sodium azide Constituents: PBS, 50% Tissue culture supernatant, 40% Glycerol (glycerin, glycerine), 0.05% BSA
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Storage information
Stable for 12 months at -20°C

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

ULK1 also known as Unc-51-like kinase 1 is a serine/threonine-protein kinase with a molecular mass of approximately 112 kDa. ULK1 is expressed in many tissues including the brain heart and skeletal muscle and plays a significant mechanical role in initializing autophagy—a process vital for cellular recycling and homeostasis. The protein interacts with several autophagy-related proteins to facilitate its functions.
Biological function summary

This protein serves as an essential part of the ULK1 complex which includes ATG13 FIP200 and ATG101. This complex acts as an important regulator in the initiation stage of autophagy responding to cellular nutrient status and energy levels. ULK1 activity promotes the formation of the phagophore which is important for capturing and degrading cytoplasmic content.

Pathways

ULK1 plays a major role in autophagy and mTOR signaling pathways. The mTOR complex 1 (mTORC1) inhibits ULK1 activity under nutrient-rich conditions preventing unnecessary autophagy. When nutrients are scarce mTORC1 inhibition releases ULK1 enhancing autophagy initiation. ULK1 also interacts with AMPK an energy-sensing kinase adjusting cellular processes according to energy levels and promoting autophagy when necessary.

Research links ULK1 to cancer and neurodegenerative diseases. Deregulation of autophagy pathways influenced by impaired ULK1 activity associates with cancer progression and tumor growth. Cancer cells often exploit autophagy to survive in nutrient-poor environments. In neurodegenerative diseases such as Alzheimer's ULK1-mediated autophagy activity can help clear protein aggregates. Understanding ULK1 interactions with proteins like AMPK in these contexts could offer advancements in therapeutic approaches.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

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, PubMed : 39384743). 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).
See full target information ULK1 pS638

Publications (4)

Recent publications for all applications. Explore the full list and refine your search

Food science & nutrition 13:e70464 PubMed40535916

2025

Ginsenoside Rh1 Alleviates Allergic Rhinitis by Mediating Mitochondrial Autophagy via Activation of the AMPK/ULK1/FUNDC1 Pathway.

Applications

Unspecified application

Species

Unspecified reactive species

Jiangang Wang,Yalin Zhang,Jingmei Chai,Jianing Yang,Longzhu Dai,Yi Yang,Yulian Zhang,Yongde Jin,Chongyang Wang,Guanghai Yan

Journal of nanobiotechnology 21:350 PubMed37759249

2023

Programmable DNA hydrogel provides suitable microenvironment for enhancing autophagy-based therapies in intervertebral disc degeneration treatment.

Applications

Unspecified application

Species

Unspecified reactive species

Song Qingxin,Jiang Kai,Zheng Dandan,Jin Linyu,Chen Xiuyuan,Feng Yubo,Wang Kun,Han Yingchao,Chen Hao,Song Jie,Chen Zhi,Shen Hongxing

Oncology letters 21:478 PubMed33968194

2021

Low CFB expression is independently associated with poor overall and disease-free survival in patients with lung adenocarcinoma.

Applications

Unspecified application

Species

Unspecified reactive species

Chenglu He,Ya Li,Ruixian Zhang,Jing Chen,Xingxing Feng,Yong Duan

Molecular medicine reports 22:2460-2468 PubMed32705220

2020

Long non‑coding RNA growth arrest‑specific 5 (GAS5) acts as a tumor suppressor by promoting autophagy in breast cancer.

Applications

Unspecified application

Species

Unspecified reactive species

Guangping Li,Lin Qian,Xiaoqin Tang,Yuan Chen,Ziyi Zhao,Cuiwei Zhang
View all publications

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