ARG55189

anti-Beclin 1 antibody

anti-Beclin 1 antibody for IHC-Formalin-fixed paraffin-embedded sections,Immunoprecipitation,Western blot and Human,Mouse,Rat

Cancer antibody; Cell Death antibody; Gene Regulation antibody; Metabolism antibody; Microbiology and Infectious Disease antibody; Autophagy Study antibody

Overview

Product Description Rabbit Polyclonal antibody recognizes Beclin 1
Tested Reactivity Hu, Ms, Rat
Tested Application IHC-P, IP, WB
Host Rabbit
Clonality Polyclonal
Isotype IgG
Target Name Beclin 1
Antigen Species Human
Immunogen Recombinant protein of Human Beclin-1 (NP_003757.1)
Conjugation Un-conjugated
Alternate Names VPS30; Beclin-1; beclin1; Coiled-coil myosin-like BCL2-interacting protein; ATG6; Protein GT197

Application Instructions

Application Suggestion
Tested Application Dilution
IHC-P1:50 - 1:200
IP1:50 - 1:100
WB1:500 - 1:2000
Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist.
Positive Control Mouse spleen and Raji

Properties

Form Liquid
Purification Affinity purification with immunogen.
Buffer PBS (pH 7.3), 0.02% Sodium azide and 50% Glycerol
Preservative 0.02% Sodium azide
Stabilizer 50% Glycerol
Storage Instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use.
Note For laboratory research only, not for drug, diagnostic or other use.

Bioinformation

Database Links

GeneID: 114558 Rat BECN1

GeneID: 56208 Mouse BECN1

GeneID: 8678 Human BECN1

Gene Symbol BECN1
Gene Full Name beclin 1, autophagy related
Background Beclin 1 regulates autophagy, a catabolic process of degradation induced by starvation. The encoded protein is a component of the phosphatidylinositol-3-kinase (PI3K) complex which mediates vesicle-trafficking processes. This protein is thought to play a role in multiple cellular processes, including tumorigenesis, neurodegeneration and apoptosis. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Sep 2015]
Function Beclin 1 plays a central role in autophagy (PubMed:23184933, PubMed:28445460). Acts as 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 abcission step in cytokinesis, probably in the context of PI3KC3-C2 (PubMed:20643123, PubMed:20208530, PubMed:26783301). Essential for the formation of PI3KC3-C2 but not PI3KC3-C1 PI3K complex forms. Involved in endocytosis (PubMed:25275521). Protects against infection by a neurovirulent strain of Sindbis virus (PubMed:9765397). 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. [UniProt]
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Research Area Cancer antibody; Cell Death antibody; Gene Regulation antibody; Metabolism antibody; Microbiology and Infectious Disease antibody; Autophagy Study antibody
Calculated MW 52 kDa
PTM Phosphorylation at Thr-119 by DAPK1 reduces its interaction with BCL2 and BCL2L1 and promotes induction of autophagy (PubMed:19180116). In response to autophagic stimuli, phosphorylated at serine residues by AMPK in an ATG14-dependent manner, and this phosphorylation is critical for maximally efficient autophagy (PubMed:23878393).
Polyubiquitinated by NEDD4, both with 'Lys11'- and 'Lys63'-linkages. 'Lys'-11-linked poyubiquitination leads to degradation and is enhanced when the stabilizing interaction partner VPS34 is depleted. Deubiquitinated by USP10 and USP13, leading to stabilize the PIK3C3/VPS34-containing complexes.
Proteolytically processed by caspases including CASP8 and CASP3; the C-terminal fragments lack autophagy-inducing capacity and are proposed to induce apoptosis. Thus the cleavage is proposed to be an determinant to switch from autophagy to apoptosis pathways affecting cellular homeostasis including viral infections and survival of tumor cells.