bim expression antibodies  (Cell Signaling Technology Inc)

 
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    Name:
    Bim Antibody
    Description:
    Bim Bod is a pro apoptotic protein belonging to the BH3 only group of Bcl 2 family members including Bad Bid Bik Hrk and Noxa that contain a BH3 domain but lack other conserved BH1 or BH2 domains 1 2 Bim induces apoptosis by binding to and antagonizing anti apoptotic members of the Bcl 2 family Interactions have been observed with Bcl 2 Bcl xL Mcl 1 Bcl w Bfl 1 and BHRF 1 1 2 Bim functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal during which Bim expression is elevated 3 6 Three major isoforms of Bim are generated by alternative splicing BimEL BimL and BimS 1 The shortest form BimS is the most cytotoxic and is generally only transiently expressed during apoptosis The BimEL and BimL isoforms may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis 7 Apoptotic activity of these longer isoforms may be regulated by phosphorylation 8 9 Environmental stress triggers Bim phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity
    Catalog Number:
    2819
    Price:
    None
    Applications:
    Western Blot, Immunoprecipitation
    Category:
    Primary Antibodies
    Source:
    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human Bim. Antibodies are purified by protein A and peptide affinity chromatography.
    Reactivity:
    Human Mouse Rat Monkey
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    Structured Review

    Cell Signaling Technology Inc bim expression antibodies
    Bim Bod is a pro apoptotic protein belonging to the BH3 only group of Bcl 2 family members including Bad Bid Bik Hrk and Noxa that contain a BH3 domain but lack other conserved BH1 or BH2 domains 1 2 Bim induces apoptosis by binding to and antagonizing anti apoptotic members of the Bcl 2 family Interactions have been observed with Bcl 2 Bcl xL Mcl 1 Bcl w Bfl 1 and BHRF 1 1 2 Bim functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal during which Bim expression is elevated 3 6 Three major isoforms of Bim are generated by alternative splicing BimEL BimL and BimS 1 The shortest form BimS is the most cytotoxic and is generally only transiently expressed during apoptosis The BimEL and BimL isoforms may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis 7 Apoptotic activity of these longer isoforms may be regulated by phosphorylation 8 9 Environmental stress triggers Bim phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity
    https://www.bioz.com/result/bim expression antibodies/product/Cell Signaling Technology Inc
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bim expression antibodies - by Bioz Stars, 2020-09
    99/100 stars

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    bcl-2
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    Related Articles

    Western Blot:

    Article Title: Combined MEK and BCL-2/XL inhibition is effective in high-grade serous ovarian cancer patient-derived xenograft models and BIM levels are predictive of responsiveness
    Article Snippet: .. Western blotting experiments were performed using BIM antibody (CST, 2933S), p-BIMS69 (CST, 4585S), p-ERKT202/T204 (Sigma, M9692), total-ERK (CST, 9102S), cleaved caspase 3 (CST, 9661L); NOXA (CST, 14766S); PUMA (CST, 4976S); β-actin (Sigma, A1978). .. For BIM knockdown experiments, siRNA oligos from Dharmacon were used (L-004383–00-0005).

    Article Title: BIM expression in treatment na?ve cancers predicts responsiveness to kinase inhibitors
    Article Snippet: .. The following antibodies used for western blots were from Cell Signaling: BIM (catalog #2819), phospho-HER2, phospho-AKT (473), phospho-ERK, phospho pras40 (246), phospho-S6 (235/236), total HER2 and total ERK. .. Other antibodies were Actin (Sigma-Aldrich); phospho-EGFR 1068 (Abcam); and total EGFR and total AKT (Santa Cruz Biotechnology).

    SDS Page:

    Article Title: Exposure to the Viral By-Product dsRNA or Coxsackievirus B5 Triggers Pancreatic Beta Cell Apoptosis via a Bim / Mcl-1 Imbalance
    Article Snippet: .. Samples were subjected to 14% SDS-PAGE gel and immunoblotted with anti-α-tubulin (Sigma), anti-Mcl-1 (Biovision) or anti-BIM antibody (Cell Signaling). .. Immunofluorescence Beta cells were plated on polylysine-coated glass culture slides (BD Biosciences).

    Immunostaining:

    Article Title: BMCC1, which is an interacting partner of BCL2, attenuates AKT activity, accompanied by apoptosis
    Article Snippet: .. Anti-Akt (no. 9272), anti-phospho-Akt (Thr308, no. 9275), anti-phospho-PDK1 (Ser241, no. 3061), anti-phospho-p53 (Ser15, no. 9284), anti-phospho-ATM (Ser1981, no. 4526), anti-phospho-Chk2 (Thr68, no. 2661), anti-caspase-9 (no. 9502), anti-caspase-6 (no. 9762), anti-BIM (no. 4582, immunoblotting), anti-BIM (no. 2933, immunostaining), anti-phospho-FOXO1/FOXO3a (Thr24/Thr32, no. 9464), anti-FOXO3a (no. 2497), anti-lamin A/C (no. 2032) and HRP-conjugated anti-rabbit (no. 7074) and anti-nmuse (no. 7076) secondary antibodies were purchased from Cell Signaling Technologies (Danvers, MA, USA). .. Antibodies purchased from Abcam (Cambridge, MA, USA) were: anti-Noxa (ab13645) antibody and an antibody raised against cleaved caspase-9 (ab52299).

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  • 90
    Cell Signaling Technology Inc rabbit anti bim
    GSK690/JNJ-26481585 cotreatment alters the balance between pro- and antiapoptotic proteins. ( a-d ) Cells were treated for indicated times with 1 μ M GSK690 (RD cells) or 10 μ M GSK690 (RH30 cells) and/or 15 nM JNJ-26481585. Expression levels of BMF, <t>BIM,</t> NOXA, and <t>PUMA</t> mRNA were analyzed by qRT-PCR and fold changes relative to untreated control of each time point are shown with mean and S.D. of three independent experiments performed in duplicate; * P
    Rabbit Anti Bim, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti bim/product/Cell Signaling Technology Inc
    Average 90 stars, based on 31 article reviews
    Price from $9.99 to $1999.99
    rabbit anti bim - by Bioz Stars, 2020-09
    90/100 stars
      Buy from Supplier

    94
    Cell Signaling Technology Inc bim
    Inhibition of PG gene expression in CRC cells enhances the expression of <t>BIM</t> in response to radiations and increases radio-induced <t>JNK</t> pathway activation BIM expression was measured, 6h post-irradiation, at the mRNA level (A, C) using real time PCR and at the protein level (B, D) by western blot analysis. Quantifications of 3 experiments are presented as means ± SD.**0.001
    Bim, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 288 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bim/product/Cell Signaling Technology Inc
    Average 94 stars, based on 288 article reviews
    Price from $9.99 to $1999.99
    bim - by Bioz Stars, 2020-09
    94/100 stars
      Buy from Supplier

    Image Search Results


    GSK690/JNJ-26481585 cotreatment alters the balance between pro- and antiapoptotic proteins. ( a-d ) Cells were treated for indicated times with 1 μ M GSK690 (RD cells) or 10 μ M GSK690 (RH30 cells) and/or 15 nM JNJ-26481585. Expression levels of BMF, BIM, NOXA, and PUMA mRNA were analyzed by qRT-PCR and fold changes relative to untreated control of each time point are shown with mean and S.D. of three independent experiments performed in duplicate; * P

    Journal: Cell Death & Disease

    Article Title: Concomitant epigenetic targeting of LSD1 and HDAC synergistically induces mitochondrial apoptosis in rhabdomyosarcoma cells

    doi: 10.1038/cddis.2017.239

    Figure Lengend Snippet: GSK690/JNJ-26481585 cotreatment alters the balance between pro- and antiapoptotic proteins. ( a-d ) Cells were treated for indicated times with 1 μ M GSK690 (RD cells) or 10 μ M GSK690 (RH30 cells) and/or 15 nM JNJ-26481585. Expression levels of BMF, BIM, NOXA, and PUMA mRNA were analyzed by qRT-PCR and fold changes relative to untreated control of each time point are shown with mean and S.D. of three independent experiments performed in duplicate; * P

    Article Snippet: Western blot analysis Western blot analysis was performed as previously described using the following antibodies: mouse anti-NOXA, rat anti-BMF, rabbit anti-MCL-1 (Enzo Life Science, Farmingdale, NY, USA), mouse anti-BCL-2, rabbit anti-BAK (BD Biosciences), rabbit anti-caspase-3, rabbit anti-caspase-9, rabbit anti-BIM, mouse anti-PARP, rabbit-anti PUMA, rabbit-anti BCL-xL (Cell Signaling, Beverly, MA, USA), mouse anti-GAPDH (HyTest, Turku, Finland), rabbit anti-H3K4me2 (Diagenode, Liège, Belgium), rabbit anti-acetylated histone H3 (Merck Millipore, Darmstadt, Germany) and mouse anti-histone H3 (Abcam) or mouse anti-β -Actin (Sigma, Germany).

    Techniques: Expressing, Quantitative RT-PCR

    Inhibition of PG gene expression in CRC cells enhances the expression of BIM in response to radiations and increases radio-induced JNK pathway activation BIM expression was measured, 6h post-irradiation, at the mRNA level (A, C) using real time PCR and at the protein level (B, D) by western blot analysis. Quantifications of 3 experiments are presented as means ± SD.**0.001

    Journal: Oncotarget

    Article Title: Targeting progastrin enhances radiosensitization of colorectal cancer cells

    doi: 10.18632/oncotarget.17274

    Figure Lengend Snippet: Inhibition of PG gene expression in CRC cells enhances the expression of BIM in response to radiations and increases radio-induced JNK pathway activation BIM expression was measured, 6h post-irradiation, at the mRNA level (A, C) using real time PCR and at the protein level (B, D) by western blot analysis. Quantifications of 3 experiments are presented as means ± SD.**0.001

    Article Snippet: Antibodies used for western blot: cleaved-PARP, cleaved-caspase 7, cleaved-caspase 8, cleaved-caspase 9, BIM, phospho-JNK, phospho-AKT, phospho-BAD-ser136, phospho-Foxo-3a-ser253, phospho-ERK, phospho-BAD-ser112, (Cell Signaling), tubulin(SIGMA), and Actin (Millipore).

    Techniques: Inhibition, Expressing, Activation Assay, Irradiation, Real-time Polymerase Chain Reaction, Western Blot

    PTEN is required for efficient upregulation of BIM following BRAF inhibition (A) WM164 cells (PTEN+) were incubated with non-targeting siRNA (NT) or transfected with two PTEN specific siRNA’s (I and II) before treatment with PLX4720 (3 or 10μM, 48hrs). Protein was resolved and probed for expression of BIM, GAPDH and PTEN. (B) Induction of PTEN-wt but not PTEN-G129E in WM793 (PTEN−) cells was sufficient to increase BIM expression when BRAF was inhibited. Left panel: Western blot shows induction of PTEN− wt and PTEN−G129E following doxycycline treatment. Right panel: Induction of PTEN-wt + PLX4720 induces BIM more efficiently than PTEN-G129E + PLX4720. (C) BIM is required for PLX4720-induced apoptosis in PTEN+ cells. WM164 and WM983A cells were incubated with non-targeting siRNA (NT) or transfected with two BIM specific siRNA’s (BIM I and BIM II) prior to treatment with PLX4720 (3 or 10μM, 48 hrs). Flow cytometry studies showed a significant reduction in TMRM loss and Annexin V binding when cells were transfected with BIM siRNA compared to non-targeting control siRNA (*P

    Journal: Cancer research

    Article Title: PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression

    doi: 10.1158/0008-5472.CAN-10-2954

    Figure Lengend Snippet: PTEN is required for efficient upregulation of BIM following BRAF inhibition (A) WM164 cells (PTEN+) were incubated with non-targeting siRNA (NT) or transfected with two PTEN specific siRNA’s (I and II) before treatment with PLX4720 (3 or 10μM, 48hrs). Protein was resolved and probed for expression of BIM, GAPDH and PTEN. (B) Induction of PTEN-wt but not PTEN-G129E in WM793 (PTEN−) cells was sufficient to increase BIM expression when BRAF was inhibited. Left panel: Western blot shows induction of PTEN− wt and PTEN−G129E following doxycycline treatment. Right panel: Induction of PTEN-wt + PLX4720 induces BIM more efficiently than PTEN-G129E + PLX4720. (C) BIM is required for PLX4720-induced apoptosis in PTEN+ cells. WM164 and WM983A cells were incubated with non-targeting siRNA (NT) or transfected with two BIM specific siRNA’s (BIM I and BIM II) prior to treatment with PLX4720 (3 or 10μM, 48 hrs). Flow cytometry studies showed a significant reduction in TMRM loss and Annexin V binding when cells were transfected with BIM siRNA compared to non-targeting control siRNA (*P

    Article Snippet: The antibodies to phospho-AKT (Ser473 and T308), total AKT, phospho-BAD (S75 and S99), Bcl-2, BIM, BRAF, FOXO3a, phospho-PDK1, total PDK1, PTEN, phospho-S6 and total S6 were from Cell Signaling Technology (Beverly, MA).

    Techniques: Inhibition, Incubation, Transfection, Expressing, Western Blot, Flow Cytometry, Cytometry, Binding Assay

    LC-MRM identifies differential regulation of BIM in PTEN+ and PTEN− cell lines following PLX4720 treatment (A) Representative LC-MRM data showing the fold-changes in the expression of Bak, Bax, Bcl-2, Bcl-w, Bcl-xL, BID, BIM, Bok and Mcl-1 over internal standard in the WM164 (PTEN+) and 1205Lu (PTEN−) cell lines following treatment with PLX4720 (10μM, 0-48 hrs). Statistical analysis of BIM fold change in PTEN− versus PTEN+, *p

    Journal: Cancer research

    Article Title: PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression

    doi: 10.1158/0008-5472.CAN-10-2954

    Figure Lengend Snippet: LC-MRM identifies differential regulation of BIM in PTEN+ and PTEN− cell lines following PLX4720 treatment (A) Representative LC-MRM data showing the fold-changes in the expression of Bak, Bax, Bcl-2, Bcl-w, Bcl-xL, BID, BIM, Bok and Mcl-1 over internal standard in the WM164 (PTEN+) and 1205Lu (PTEN−) cell lines following treatment with PLX4720 (10μM, 0-48 hrs). Statistical analysis of BIM fold change in PTEN− versus PTEN+, *p

    Article Snippet: The antibodies to phospho-AKT (Ser473 and T308), total AKT, phospho-BAD (S75 and S99), Bcl-2, BIM, BRAF, FOXO3a, phospho-PDK1, total PDK1, PTEN, phospho-S6 and total S6 were from Cell Signaling Technology (Beverly, MA).

    Techniques: Expressing

    Loss of BMF or BIM increases anoikis resistance of E-cadherin-expressing breast cancer cells. ( a and b ) Knockdown of BMF and BIM reduces apoptosis of Trp53 Δ/Δ and MCF7 cells cultured in Sus. Flow cytometric quantifications of apoptosis

    Journal: Cell Death and Differentiation

    Article Title: Restraining FOXO3-dependent transcriptional BMF activation underpins tumour growth and metastasis of E-cadherin-negative breast cancer

    doi: 10.1038/cdd.2016.33

    Figure Lengend Snippet: Loss of BMF or BIM increases anoikis resistance of E-cadherin-expressing breast cancer cells. ( a and b ) Knockdown of BMF and BIM reduces apoptosis of Trp53 Δ/Δ and MCF7 cells cultured in Sus. Flow cytometric quantifications of apoptosis

    Article Snippet: Proteins were detected using SDS-PAGE and subsequent western blotting analysis with primary antibodies recognising BAD (CST-9292, Cell Signaling Technology, Leiden, The Netherlands), BIM (CST-2819) BMF (human: CST-5889, mouse: ENZO-17A9), BID (SC-11423 Santa Cruz, Heidelberg, Germany), AKT/PKB (CST), FOXO1 (CST- 29H4), FOXO3 (H144 Santa Cruz), NOXA (SP7122p Acris, Herford, Germany), PUMA (CST-4976) and BCL2 (CST-2876) used at 1 : 2000.

    Techniques: Expressing, Cell Culture, Flow Cytometry