Product: Beclin 1 Antibody
Catalog: AF5128
Description: Rabbit polyclonal antibody to Beclin 1
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 52 kDa; 52kD(Calculated).
Uniprot: Q14457
RRID: AB_2837614

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Zebrafish(93%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(93%)
Clonality:
Polyclonal
Specificity:
Beclin 1 Antibody detects endogenous levels of total Beclin 1.
RRID:
AB_2837614
Cite Format: Affinity Biosciences Cat# AF5128, RRID:AB_2837614.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

APG6; ATG 6; ATG6; ATG6 autophagy related 6 homolog; Bcl-2-interacting protein beclin; Beclin 1 (coiled coil moesin like BCL2 interacting protein); Beclin 1 autophagy related; Beclin-1; Beclin1; BECN 1; Becn1; BECN1_HUMAN; Coiled coil myosin like BCL2 interacting protein; Coiled-coil myosin-like BCL2-interacting protein; GT197; Protein GT197; VPS 30; VPS30;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
Q14457 BECN1_HUMAN:

Ubiquitous.

Description:
Plays a central role in autophagy (By similarity). May play a role in antiviral host defense. Protects against infection by a neurovirulent strain of Sindbis virus.
Sequence:
MEGSKTSNNSTMQVSFVCQRCSQPLKLDTSFKILDRVTIQELTAPLLTTAQAKPGETQEEETNSGEEPFIETPRQDGVSRRFIPPARMMSTESANSFTLIGEASDGGTMENLSRRLKVTGDLFDIMSGQTDVDHPLCEECTDTLLDQLDTQLNVTENECQNYKRCLEILEQMNEDDSEQLQMELKELALEEERLIQELEDVEKNRKIVAENLEKVQAEAERLDQEEAQYQREYSEFKRQQLELDDELKSVENQMRYAQTQLDKLKKTNVFNATFHIWHSGQFGTINNFRLGRLPSVPVEWNEINAAWGQTVLLLHALANKMGLKFQRYRLVPYGNHSYLESLTDKSKELPLYCSGGLRFFWDNKFDHAMVAFLDCVQQFKEEVEKGETRFCLPYRMDVEKGKIEDTGGSGGSYSIKTQFNSEEQWTKALKFMLTNLKWGLAWVSSQFYNK

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Chicken
100
Rabbit
100
Xenopus
93
Zebrafish
93
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q14457 As Substrate

Site PTM Type Enzyme
Ubiquitination
M1 Acetylation
S15 Phosphorylation
K26 Ubiquitination
S30 Phosphorylation
K32 Ubiquitination
T38 Phosphorylation
K53 Ubiquitination
T57 Phosphorylation
T62 Phosphorylation
S64 Phosphorylation
S90 Phosphorylation P49137 (MAPKAPK2) , Q16644 (MAPKAPK3)
T91 Phosphorylation
S93 Phosphorylation
S96 Phosphorylation
T108 Phosphorylation Q13043 (STK4)
K117 Ubiquitination
T119 Phosphorylation P53355 (DAPK1)
T141 Phosphorylation
K203 Ubiquitination
K206 Acetylation
K214 Ubiquitination
Y229 Phosphorylation P00533 (EGFR)
Y233 Phosphorylation P00533 (EGFR)
S234 Phosphorylation
K237 Ubiquitination
K248 Ubiquitination
K263 Ubiquitination
S279 Phosphorylation
S295 Phosphorylation P31749 (AKT1)
K324 Ubiquitination
S337 Phosphorylation
Y352 Phosphorylation P00533 (EGFR)
T388 Phosphorylation
K402 Ubiquitination
T406 Phosphorylation P78368 (CSNK1G2)
S409 Phosphorylation P78368 (CSNK1G2)
K427 Ubiquitination
K430 Acetylation
K437 Acetylation
K437 Ubiquitination

Research Backgrounds

Function:

Plays a central role in autophagy. 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. Essential for the formation of PI3KC3-C2 but not PI3KC3-C1 PI3K complex forms. Involved in endocytosis. Protects against infection by a neurovirulent strain of Sindbis virus. 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.

PTMs:

Phosphorylation at Thr-119 by DAPK1 reduces its interaction with BCL2 and BCL2L1 and promotes induction of autophagy. 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.

Polyubiquitinated by NEDD4, both with 'Lys-11'- and 'Lys-63'-linkages. 'Lys-11'-linked polyubiquitination 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. Polyubiquitinated at Lys-402 with 'Lys-48'-linkages. 'Lys-48'-linked polyubiquitination of Lys-402 leads to degradation. Deubiquitinated by ATXN3, leading to stabilization.

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.

Subcellular Location:

Cytoplasm. Golgi apparatus>trans-Golgi network membrane>Peripheral membrane protein. Endosome membrane>Peripheral membrane protein. Endoplasmic reticulum membrane>Peripheral membrane protein. Mitochondrion membrane>Peripheral membrane protein. Endosome. Cytoplasmic vesicle>Autophagosome.
Note: Interaction with ATG14 promotes translocation to autophagosomes. Expressed in dendrites and cell bodies of cerebellar Purkinje cells (By similarity).

Mitochondrion. Nucleus. Cytoplasm.

Mitochondrion.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Ubiquitous.

Subunit Structure:

A homodimeric form is proposed to exist; this metastable form readily transits to ATG14- or UVRAG-containing complexes with BECN1:UVRAG being more stable than BECN1:ATG14 (By similarity). Component of the PI3K (PI3KC3/PI3K-III/class III phosphatidylinositol 3-kinase) complex the core of which is composed of the catalytic subunit PIK3C3, the regulatory subunit PIK3R4 and BECN1 associating with additional regulatory/auxilliary subunits to form alternative complex forms. Alternative complex forms containing a forth regulatory subunit in a mutually exclusive manner are PI3K complex I (PI3KC3-C1) containing ATG14, and PI3K complex II (PI3KC3-C2) containing UVRAG. PI3KC3-C1 displays a V-shaped architecture with PIK3R4 serving as a bridge between PIK3C3 and the ATG14:BECN1 subcomplex. Both, PI3KC3-C1 and PI3KC3-C2, can associate with further regulatory subunits, such as RUBCN, SH3GLB1/Bif-1 and AMBRA1. PI3KC3-C1 probably associates with PIK3CB (By similarity). Interacts with AMBRA1, GOPC, GRID2 (By similarity). Interacts with BCL2 and BCL2L1 isoform Bcl-X(L); the interaction inhibits BECN1 function in promoting autophagy by interfering with the formation of the PI3K complex. Interacts with cytosolic HMGB1; inhibits the interaction of BECN1 and BCL2 leading to promotion of autophagy. Interacts with USP10, USP13, VMP1, DAPK1, RAB39A. Interacts with the poly-Gln domain of ATXN3; the interaction causes deubiquitination at Lys-402 and stabilizes BECN1. Interacts with SLAMF1. Interacts with TRIM5; the interaction causes activation of BECN1 by causing its dissociation from its inhibitors BCL2 and TAB2. Interacts with active ULK1 (phosphorylated on 'Ser-317') and MEFV simultaneously. Interacts with WDR81 and WDR91; negatively regulates the PI3 kinase/PI3K activity associated with endosomal membranes. Interacts with LAPTM4B; competes with EGFR for LAPTM4B binding; regulates EGFR activity. Interacts with TRIM50. Interacts with TRIM16.

(Microbial infection) Interacts with human cytomegalovirus/HHV-5 protein TRS1.

(Microbial infection) Interacts with murine gammaherpesvirus 68 M11.

(Microbial infection) Interacts with herpes simplex virus 1 (HHV-1) protein ICP34.5; this interaction antagonizes the host autophagy response.

Family&Domains:

The coiled coil domain can form antiparallel homodimers and mediates dimerization with the coiled coil domains of ATG14 or UVRAG involved in the formation of PI3K complexes.

The C-terminal evolutionary conserved domain (ECD) contains poly-Gln-binding domains such as the ATXN3 poly-Gln motif, consistent with structural docking models revealing two highly scored poly-Gln-binding pockets in the ECD (PubMed:28445460). As some binding is observed with BECN1 lacking the ECD, other domains of BECN1 may also interact with ATXN3 (PubMed:28445460).

Belongs to the beclin family.

Research Fields

· Cellular Processes > Transport and catabolism > Autophagy - other.   (View pathway)

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

References

1). Gold nanoparticles targeting the autophagy–lysosome system to combat the inflammation-compromised osteogenic potential of periodontal ligament stem cells: From mechanism to therapy. Biomaterials, 2022 (PubMed: 36030103) [IF=14.0]

2). NCAPD2 inhibits autophagy by regulating Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis to promote colorectal cancer. CANCER LETTERS, 2021 (PubMed: 34229059) [IF=9.7]

Application: WB    Species: Human    Sample: CRC cells

Fig. 2. NCAPD2 inhibited cell autophagy and disrupted autophagic flux via Ca2+/CAMKK2/AMPK/mTORC1 pathway. (A) Western blot analyses for phosphorylated mTOR (p-mTOR, S2448), phosphorylated p70S6K (p-p70S6K, T389/412), phosphorylated 4E-BP1 (p-4E-BP1, T70) and phosphorylated AKT (p-AKT, S473) in CRCC cells with different treatments as indicated. (B) Western blot of indicated proteins in cells treated with mTORC1 inhibitor Rapamycin (3 nM, 24h). (C) Immunofluorescence staining of LC3II (red) and P62 (red) in CRC cells with different treatments as indicated. Merged images represented overlays of LC3II or P62 and nuclear staining by DAPI (blue). (D) Intracellular Ca2+ levels were analyzed by flow cytometry after staining with the fluorescent probe Fluo-3, AM in CRC cells. (E) Representative Western blot gel documents of phosphorylated CAMKK2(S511), phosphorylated AMPK(T172), phosphorylated mTOR(S2448), Beclin, ATG5, P62, LC3II in CRC cells with different treatments. (F) Western blots of indicated proteins in cells treated with an inhibitor of microsomal Ca2+-ATPase Thapsigargin (1 μM, 6h) and Ca2+ chelator BAPTA-AM (10 μM, 12h) respectively. Results are shown as mean ± s.d, *P < 0.05, **P < 0.01, ***P < 0.001, based on Student’s t-test. . (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

3). Polysaccharide from Strongylocentrotus nudus eggs regulates intestinal epithelial autophagy through CD36/PI3K-Akt pathway to ameliorate inflammatory bowel disease. International Journal of Biological Macromolecules, 2023 (PubMed: 37327932) [IF=8.2]

4). d-Borneol enhances cisplatin sensitivity via autophagy dependent EMT signaling and NCOA4-mediated ferritinophagy. PHYTOMEDICINE, 2022 (PubMed: 36030746) [IF=7.9]

5). MiR-34a inhibitor protects mesenchymal stem cells from hyperglycaemic injury through the activation of the SIRT1/FoxO3a autophagy pathway. Stem Cell Research & Therapy, 2020 (PubMed: 33546760) [IF=7.5]

Application: WB    Species: mouse    Sample: MSCs

Fig. 3 |MiR-34a influences the expression of autophagy factors under hyperglycaemic conditions. MSCs were cultured with normal or high glucose medium for 28 days with or without transfection with miR-34a mimic, NC or miR-34a inhibitor for 48 h, respectively. a, b The protein level of SIRT1 and FoxO3a, and autophagy-related protein LC3 and Beclin1 were determined by western blot.

6). Huaier polysaccharides suppress triple-negative breast cancer metastasis and epithelial-mesenchymal transition by inducing autophagic degradation of Snail. Cell and Bioscience, 2021 (PubMed: 34481526) [IF=7.5]

Application: WB    Species: human    Sample: MDA-MB-231 cells

Fig. 2 |PS-T reverses EMT by inducing autophagy. a MDA-MB-231 cells are treated with 5 μg/mL PS-T for 24 h. The levels of each autophagy marker in MDA-MB-231 cells are quantifed using the NIH ImageJ software. (mean ± SD, *P < 0.05 and ***P < 0.001).

Application: WB    Species: Human    Sample: MDA-MB-231 cells

Fig. 2 PS-T reverses EMT by inducing autophagy. a MDA-MB-231 cells are treated with 5 μg/mL PS-T for 24 h. The levels of each autophagy marker in MDA-MB-231 cells are quantified using the NIH ImageJ software. (mean  ±  SD, *P  <  0.05 and ***P  <  0.001). b Confocal microscopy images of cells treated with or without PS-T (5 μg/mL) for 24 h after transfection with mRFP-GFP-LC3 plasmid (scale bars: 10 μm). Quantification of LC3-GFP and LC3-RFP puncta/cells from three independent experiments (***P  <  0.001). c MDA-MB-231 cells are treated with PS-T (5 μg/mL) for 24 h with or without LY294002 (10 µM). The levels of each EMT marker in MDA-MB-231cells were quantified using NIH ImageJ software. (mean  ±  SD, *P  <  0.05 and **P  <  0.01)

7). RETRACTED ARTICLE: MiR-34a inhibitor protects mesenchymal stem cells from hyperglycaemic injury through the activation of the SIRT1/FoxO3a autophagy pathway. Stem Cell Research & Therapy, 2021 (PubMed: 33546760) [IF=7.5]

Application: WB    Species: Rat    Sample:

Fig. 3 MiR-34a influences the expression of autophagy factors under hyperglycaemic conditions. MSCs were cultured with normal or high glucose medium for 28 days with or without transfection with miR-34a mimic, NC or miR-34a inhibitor for 48 h, respectively. a, b The protein level of SIRT1 and FoxO3a, and autophagy-related protein LC3 and Beclin1 were determined by western blot. c Autophagic corpuscle was detected by TEM. Data are presented as mean ± SD of three separate experiments. *P 

8). Geniposide ameliorates glucocorticoid-induced osteoblast apoptosis by activating autophagy. Biomedicine & Pharmacotherapy, 2022 (PubMed: 36271582) [IF=7.5]

Application: WB    Species: Rat    Sample: MC3T3-E1 cells

Fig. 3. The effects of GEN on autophagy in DEX-treated osteoblasts in vivo and in vitro. The immunohistochemical changes (× 40 magnification) of P62 (A, B), LC3-II (A, C), and Beclin-1 (A, D) were analyzed. The proteins expression of P62 (E, F), LC3-II (E, G), and Beclin-1 (E, H) in DEX-treated MC3T3-E1 cells were determined by western blot. * *P˂0.01. NC, negative control group; DEX, model rat group treated with DEX (5 mg/kg).

Application: IHC    Species: Rat    Sample: MC3T3-E1 cells

Fig. 3. The effects of GEN on autophagy in DEX-treated osteoblasts in vivo and in vitro. The immunohistochemical changes (× 40 magnification) of P62 (A, B), LC3-II (A, C), and Beclin-1 (A, D) were analyzed. The proteins expression of P62 (E, F), LC3-II (E, G), and Beclin-1 (E, H) in DEX-treated MC3T3-E1 cells were determined by western blot. * *P˂0.01. NC, negative control group; DEX, model rat group treated with DEX (5 mg/kg).

9). Activation of aldehyde dehydrogenase-2 improves ischemic random skin flap survival in rats. Frontiers in Immunology, 2023 (PubMed: 37441072) [IF=7.3]

Application: IF/ICC    Species: Mouse    Sample:

Figure 10 Immunofluorescence images of Beclin-1 (A), p62 (B), and LC3(C) were captured under fluorescence microscopy, and the relative fluorescence intensity was calculated. All images were obtained at identical magnification, ×200, scale bar = 50 μm. Data are represented as mean ± SEM (n = 3). **P

10). A Potent Protective Effect of Baicalein on Liver Injury by Regulating Mitochondria-Related Apoptosis. APOPTOSIS, 2020 (PubMed: 32409930) [IF=7.2]

Application: WB    Species: human    Sample: L02 cells

Fig. 4| Protective efect of baicalein on H­2O2 induced hepatotoxicity. L02 cells were pre-treated with 100 μM H­2O2 for 1 h, then co-incubated with 50 μM baicalein for 11 h. a Mitochondrial and apoptosis were stained with MitoTracker Red and TUNEL, respectively. b The percentage of cells underwent mitochondrial fssion and TUNEL positive cell. c The expression levels of apoptotic and autophagy related proteins were detected by western blotting and densitometry.

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