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AB183335

Anti-Beclin 1 (phospho S234) antibody

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(7 Publications)

Rabbit Polyclonal Beclin 1 phospho S234 antibody. Suitable for WB and reacts with Human samples. Cited in 7 publications. Immunogen corresponding to Synthetic Peptide within Human BECN1 pS234.

View Alternative Names

GT197, BECN1, Beclin-1, Coiled-coil myosin-like BCL2-interacting protein, Protein GT197

1 Images
Western blot - Anti-Beclin 1 (phospho S234) antibody (AB183335)
  • WB

Supplier Data

Western blot - Anti-Beclin 1 (phospho S234) antibody (AB183335)

All lanes:

Western blot - Anti-Beclin 1 (phospho S234) antibody (ab183335) at 1/250 dilution

Lane 1:

Lysate from 293T cells expressing wild type flag-Beclin 1

Lane 2:

Lysate from 293T cells expressing mutant flag-Beclin 1 (S234A, S295A)

Predicted band size: 52 kDa

Observed band size: 60 kDa

false

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

WB

applications

Immunogen

Synthetic Peptide within Human BECN1 pS234. The exact immunogen used to generate this antibody is proprietary information.

Q14457

Specificity

Immunolabeling of the Beclin 1 band is decreased in the Beclin 1 alanine substitution mutant. Additional bands may be observed in non-immunoprecipitated lysates.

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Purification notes
ab183335 was prepared from rabbit serum by affinity purification via sequential chromatography on phospho- and dephosphopeptide affinity column.
Storage buffer
pH: 7.5 Constituents: 50% Glycerol (glycerin, glycerine), 0.88% Sodium chloride, 0.24% HEPES, 0.01% BSA
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

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

Beclin 1 sometimes referred to as beclin-1 or becn1 is a protein that plays a mechanical role in autophagy. This process involves the recycling of cellular components and is essential for maintaining cellular health. Beclin 1 is approximately 60 kDa in molecular weight and is expressed in a variety of tissues throughout the body. It acts at the molecular level engaging in the initial stages of autophagosome formation which are critical for cell survival during nutrient deprivation.
Biological function summary

The protein functions as an important component of the Beclin 1 autophagy complex which orchestrates the autophagic process. This complex is essential for promoting autophagosome nucleation by interacting with multiple partners that regulate the autophagy pathway. In addition to its role in autophagy Beclin 1 protein stabilizes interactions with other autophagic proteins ensuring the correct assembly and activity of this cellular mechanism. The regulation of Beclin 1's activity and expression influences the efficiency and specificity of autophagy in cells.

Pathways

Beclin 1 integrates into critical cellular pathways like the PI3K/Akt pathway and the mTOR pathway which are pivotal in cell growth and survival. Within these pathways beclin cooperates closely with proteins such as ATG14 and VPS34. These interactions facilitate the recruitment and activation of additional factors that promote the elongation of phagophores which eventually become complete autophagosomes. The coordination of these pathways ensures the proper balance between cell survival and death adapting to cellular conditions.

Beclin 1 shows significant relevance in cancer and neurodegenerative diseases. Abnormal Beclin 1 expression and function are linked to a range of cancers as its dysregulation affects apoptosis and autophagic turnover. Furthermore in neurodegenerative disorders like Alzheimer's disease altered Beclin 1 activity can disrupt normal protein degradation exacerbating protein aggregation a hallmark of these conditions. Interactions with proteins like Bcl-2 are essential in the context of these diseases as Bcl-2 modulates the autophagic and apoptotic balance directly impacting disease progression.

Product protocols

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

Target data

Plays a central role in autophagy (PubMed : 18570871, PubMed : 21358617, PubMed : 23184933, PubMed : 23974797, PubMed : 25484083, PubMed : 28445460, PubMed : 37776275). Acts as a core 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. 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, PubMed : 23974797, PubMed : 26783301). Essential for the formation of PI3KC3-C2 but not PI3KC3-C1 PI3K complex forms. Involved in endocytosis (PubMed : 25275521). May play a role in antiviral host defense.. Beclin-1-C 35 kDa localized to mitochondria can promote apoptosis; it induces the mitochondrial translocation of BAX and the release of proapoptotic factors.. (Microbial infection) Protects against infection by a neurovirulent strain of Sindbis virus.
See full target information BECN1 pS234

Publications (7)

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

Molecular and cellular biochemistry 478:1415-1425 PubMed36348200

2022

The protective effects of melatonin in high glucose environment by alleviating autophagy and apoptosis on primary cortical neurons.

Applications

Unspecified application

Species

Unspecified reactive species

Lijiao Xiong,Song Liu,Chaoming Liu,Tianting Guo,Zhihua Huang,Liangdong Li

Annals of translational medicine 9:1545 PubMed34790751

2021

miR-17-5p attenuates kidney ischemia-reperfusion injury by inhibiting the PTEN and BIM pathways.

Applications

Unspecified application

Species

Unspecified reactive species

Ming Ma,Lei Fu,Zihao Jia,Qiang Zhong,Zhongli Huang,Xianding Wang,Yu Fan,Tao Lin,Turun Song

International journal of molecular medicine 43:1311-1320 PubMed30747228

2019

Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1.

Applications

Unspecified application

Species

Unspecified reactive species

Pan Tan,Haiqin Wang,Junkun Zhan,Xinyu Ma,Xingjun Cui,Yanjiao Wang,Yi Wang,Jiayu Zhong,Youshuo Liu

Scientific reports 8:615 PubMed29330382

2018

SESN2 facilitates mitophagy by helping Parkin translocation through ULK1 mediated Beclin1 phosphorylation.

Applications

Unspecified application

Species

Unspecified reactive species

Ashish Kumar,Chandrima Shaha

International journal of molecular medicine 39:559-568 PubMed28112381

2017

Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway.

Applications

Unspecified application

Species

Human

Guodong Huang,Bingyu Zou,Jianzhen Lv,Tongyu Li,Guoli Huai,Shaowei Xiang,Shilong Lu,Huan Luo,Yaping Zhang,Yi Jin,Yi Wang

International journal of molecular medicine 37:309-18 PubMed26647915

2015

Electroacupuncture protects against ischemic stroke by reducing autophagosome formation and inhibiting autophagy through the mTORC1-ULK1 complex-Beclin1 pathway.

Applications

WB

Species

Unspecified reactive species

Weilin Liu,Guanhao Shang,Shanli Yang,Jia Huang,Xiehua Xue,Yunjiao Lin,Yi Zheng,Xian Wang,Lulu Wang,Ruhui Lin,Jing Tao,Lidian Chen

PloS one 9:e101526 PubMed24992302

2014

Molecular switch role of Akt in Polygonatum odoratum lectin-induced apoptosis and autophagy in human non-small cell lung cancer A549 cells.

Applications

WB

Species

Human

Chunyang Li,Jie Chen,Bangmin Lu,Zheng Shi,Hailian Wang,Bin Zhang,Kailiang Zhao,Wei Qi,Jinku Bao,Yi Wang
View all publications

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