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anti bcl 2 d17c4 rabbit mab  (Cell Signaling Technology Inc)
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Antibodies Used in the Study.
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Fig. 8 | Schematic representation of the mechan- isms underlying the toxicity caused by co- expression of ASCL1 and NEUROD1 in SCLC cells. (Top) SCLC-A and SCLC-N cells are primarily driven by the lineage-specific transcrip- tion factors, ASCL1 or NEUROD1, respectively. (Bottom) In SCLC-A cells, co-expression of NEU- ROD1 leads to suppression of ASCL1, down- regulation of ASCL1 target genes, and upregulation of NEUROD1 target genes. This process is accom- panied by genome-wide changes in chromatin accessibility. NEUROD1 co-expression induces caspase-dependent apoptotic cell death by directly repressing the anti-apoptotic protein, <t>BCL2,</t> with additional repression of its upstream regulator, ASCL1, further reinforcing this effect (left). In SCLC-N cells, co-expressed ASCL1 suppresses NEUROD1 and reciprocally, but with greater effi- ciency, downregulates NEUROD1 target genes while upregulating ASCL1 target genes, with notable changes in the chromatin accessibility landscape. In these cells, apoptosis induced by ASCL1 co- expression involves both caspase-dependent and -independent mechanisms (right).
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Image Search Results


Antibodies Used in the Study.

Journal: Journal of Histochemistry and Cytochemistry

Article Title: Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes

doi: 10.1369/0022155417722118

Figure Lengend Snippet: Antibodies Used in the Study.

Article Snippet: No Source CDK2 Rabbit, polyclonal PB0562 Boster phospho(p)-CDK2 Rabbit, polyclonal BM4590 Boster cyclin D1 Rabbit, polyclonal BA0770 Boster p-cyclin D1 Rabbit, polyclonal BM4272 Boster p53 Rabbit, polyclonal {"type":"entrez-nucleotide","attrs":{"text":"A00001","term_id":"58418","term_text":"A00001"}} A00001 Boster p21 Waf1/Cip1 Rabbit, polyclonal BM4382 Boster Bcl-2 Rabbit, polyclonal D17C4 Cell Signaling Technology Bcl-xl Rabbit, polyclonal 54H6 Cell Signaling Technology p-PI3K Rabbit, polyclonal 4228S Cell Signaling Technology PI3K Rabbit, polyclonal 4249S Cell Signaling Technology p-p38 MAPK Rabbit, polyclonal 8690S Cell Signaling Technology p38 MAPK Rabbit, polyclonal 7257s Cell Signaling Technology p-Akt (Ser473) Rabbit, polyclonal 4060S Cell Signaling Technology Akt Rabbit, polyclonal 4691S Cell Signaling Technology p-mTOR Rabbit, polyclonal 5536S Cell Signaling Technology mTOR Rabbit, polyclonal 2983S Cell Signaling Technology Beclin 1 Rabbit, polyclonal 3495S Cell Signaling Technology LC3-I/II Rabbit, polyclonal 12741S Cell Signaling Technology p62 Rabbit, polyclonal 8025S Cell Signaling Technology PTEN Rabbit, polyclonal 9188S Cell Signaling Technology p-AMPK Rabbit, polyclonal 2537S Cell Signaling Technology AMPK Rabbit, polyclonal 4150S Cell Signaling Technology 4EBP1 Rabbit, polyclonal 9644S Cell Signaling Technology p-4EBP Rabbit, monoclonal 2855S Cell Signaling Technology p-P70S6K Rabbit, monoclonal 9204S Cell Signaling Technology Open in a separate window Antibodies Used in the Study.

Techniques:

Effect of Euptox A on the expression or phosphorylation levels of key autophagy-regulating molecules in splenocytes. (A) Representative blots show the protein levels of PI3K, Akt, and mTOR, and the phosphorylation of PI3K, Akt T37/46, AMPK, p38 MAPK, mTOR S2448, p70S60K, and 4EBP1 in splenocytes administered with Euptox A. (B) Bar graphs show the ratio of p-PI3K/PI3K, p-AMPK/AMPK, p-Akt/Akt, p-p38 MAPK/p38 MAPK, p-mTOR/mTOR, and the expression levels of PTEN in splenocytes. β-Actin was used as the internal control. Data are presented with the means ± SD and mean values of three independent experiments. *p<0.05, compared with the control group; **p<0.01, compared with the control group.

Journal: Journal of Histochemistry and Cytochemistry

Article Title: Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes

doi: 10.1369/0022155417722118

Figure Lengend Snippet: Effect of Euptox A on the expression or phosphorylation levels of key autophagy-regulating molecules in splenocytes. (A) Representative blots show the protein levels of PI3K, Akt, and mTOR, and the phosphorylation of PI3K, Akt T37/46, AMPK, p38 MAPK, mTOR S2448, p70S60K, and 4EBP1 in splenocytes administered with Euptox A. (B) Bar graphs show the ratio of p-PI3K/PI3K, p-AMPK/AMPK, p-Akt/Akt, p-p38 MAPK/p38 MAPK, p-mTOR/mTOR, and the expression levels of PTEN in splenocytes. β-Actin was used as the internal control. Data are presented with the means ± SD and mean values of three independent experiments. *p<0.05, compared with the control group; **p<0.01, compared with the control group.

Article Snippet: No Source CDK2 Rabbit, polyclonal PB0562 Boster phospho(p)-CDK2 Rabbit, polyclonal BM4590 Boster cyclin D1 Rabbit, polyclonal BA0770 Boster p-cyclin D1 Rabbit, polyclonal BM4272 Boster p53 Rabbit, polyclonal {"type":"entrez-nucleotide","attrs":{"text":"A00001","term_id":"58418","term_text":"A00001"}} A00001 Boster p21 Waf1/Cip1 Rabbit, polyclonal BM4382 Boster Bcl-2 Rabbit, polyclonal D17C4 Cell Signaling Technology Bcl-xl Rabbit, polyclonal 54H6 Cell Signaling Technology p-PI3K Rabbit, polyclonal 4228S Cell Signaling Technology PI3K Rabbit, polyclonal 4249S Cell Signaling Technology p-p38 MAPK Rabbit, polyclonal 8690S Cell Signaling Technology p38 MAPK Rabbit, polyclonal 7257s Cell Signaling Technology p-Akt (Ser473) Rabbit, polyclonal 4060S Cell Signaling Technology Akt Rabbit, polyclonal 4691S Cell Signaling Technology p-mTOR Rabbit, polyclonal 5536S Cell Signaling Technology mTOR Rabbit, polyclonal 2983S Cell Signaling Technology Beclin 1 Rabbit, polyclonal 3495S Cell Signaling Technology LC3-I/II Rabbit, polyclonal 12741S Cell Signaling Technology p62 Rabbit, polyclonal 8025S Cell Signaling Technology PTEN Rabbit, polyclonal 9188S Cell Signaling Technology p-AMPK Rabbit, polyclonal 2537S Cell Signaling Technology AMPK Rabbit, polyclonal 4150S Cell Signaling Technology 4EBP1 Rabbit, polyclonal 9644S Cell Signaling Technology p-4EBP Rabbit, monoclonal 2855S Cell Signaling Technology p-P70S6K Rabbit, monoclonal 9204S Cell Signaling Technology Open in a separate window Antibodies Used in the Study.

Techniques: Expressing

Expression of LC3-II, p62, p-PI3K, p-AKT, p-mTOR, and PTEN protein in the splenocytes. Scale bar = 20 µm. Abbreviation: NC, negative control.

Journal: Journal of Histochemistry and Cytochemistry

Article Title: Euptox A Induces G1 Arrest and Autophagy via p38 MAPK- and PI3K/Akt/mTOR-Mediated Pathways in Mouse Splenocytes

doi: 10.1369/0022155417722118

Figure Lengend Snippet: Expression of LC3-II, p62, p-PI3K, p-AKT, p-mTOR, and PTEN protein in the splenocytes. Scale bar = 20 µm. Abbreviation: NC, negative control.

Article Snippet: No Source CDK2 Rabbit, polyclonal PB0562 Boster phospho(p)-CDK2 Rabbit, polyclonal BM4590 Boster cyclin D1 Rabbit, polyclonal BA0770 Boster p-cyclin D1 Rabbit, polyclonal BM4272 Boster p53 Rabbit, polyclonal {"type":"entrez-nucleotide","attrs":{"text":"A00001","term_id":"58418","term_text":"A00001"}} A00001 Boster p21 Waf1/Cip1 Rabbit, polyclonal BM4382 Boster Bcl-2 Rabbit, polyclonal D17C4 Cell Signaling Technology Bcl-xl Rabbit, polyclonal 54H6 Cell Signaling Technology p-PI3K Rabbit, polyclonal 4228S Cell Signaling Technology PI3K Rabbit, polyclonal 4249S Cell Signaling Technology p-p38 MAPK Rabbit, polyclonal 8690S Cell Signaling Technology p38 MAPK Rabbit, polyclonal 7257s Cell Signaling Technology p-Akt (Ser473) Rabbit, polyclonal 4060S Cell Signaling Technology Akt Rabbit, polyclonal 4691S Cell Signaling Technology p-mTOR Rabbit, polyclonal 5536S Cell Signaling Technology mTOR Rabbit, polyclonal 2983S Cell Signaling Technology Beclin 1 Rabbit, polyclonal 3495S Cell Signaling Technology LC3-I/II Rabbit, polyclonal 12741S Cell Signaling Technology p62 Rabbit, polyclonal 8025S Cell Signaling Technology PTEN Rabbit, polyclonal 9188S Cell Signaling Technology p-AMPK Rabbit, polyclonal 2537S Cell Signaling Technology AMPK Rabbit, polyclonal 4150S Cell Signaling Technology 4EBP1 Rabbit, polyclonal 9644S Cell Signaling Technology p-4EBP Rabbit, monoclonal 2855S Cell Signaling Technology p-P70S6K Rabbit, monoclonal 9204S Cell Signaling Technology Open in a separate window Antibodies Used in the Study.

Techniques: Expressing, Negative Control

Fig. 8 | Schematic representation of the mechan- isms underlying the toxicity caused by co- expression of ASCL1 and NEUROD1 in SCLC cells. (Top) SCLC-A and SCLC-N cells are primarily driven by the lineage-specific transcrip- tion factors, ASCL1 or NEUROD1, respectively. (Bottom) In SCLC-A cells, co-expression of NEU- ROD1 leads to suppression of ASCL1, down- regulation of ASCL1 target genes, and upregulation of NEUROD1 target genes. This process is accom- panied by genome-wide changes in chromatin accessibility. NEUROD1 co-expression induces caspase-dependent apoptotic cell death by directly repressing the anti-apoptotic protein, BCL2, with additional repression of its upstream regulator, ASCL1, further reinforcing this effect (left). In SCLC-N cells, co-expressed ASCL1 suppresses NEUROD1 and reciprocally, but with greater effi- ciency, downregulates NEUROD1 target genes while upregulating ASCL1 target genes, with notable changes in the chromatin accessibility landscape. In these cells, apoptosis induced by ASCL1 co- expression involves both caspase-dependent and -independent mechanisms (right).

Journal: NPJ precision oncology

Article Title: Lethal co-expression intolerance underlies the mutually exclusive expression of ASCL1 and NEUROD1 in SCLC cells.

doi: 10.1038/s41698-025-00860-6

Figure Lengend Snippet: Fig. 8 | Schematic representation of the mechan- isms underlying the toxicity caused by co- expression of ASCL1 and NEUROD1 in SCLC cells. (Top) SCLC-A and SCLC-N cells are primarily driven by the lineage-specific transcrip- tion factors, ASCL1 or NEUROD1, respectively. (Bottom) In SCLC-A cells, co-expression of NEU- ROD1 leads to suppression of ASCL1, down- regulation of ASCL1 target genes, and upregulation of NEUROD1 target genes. This process is accom- panied by genome-wide changes in chromatin accessibility. NEUROD1 co-expression induces caspase-dependent apoptotic cell death by directly repressing the anti-apoptotic protein, BCL2, with additional repression of its upstream regulator, ASCL1, further reinforcing this effect (left). In SCLC-N cells, co-expressed ASCL1 suppresses NEUROD1 and reciprocally, but with greater effi- ciency, downregulates NEUROD1 target genes while upregulating ASCL1 target genes, with notable changes in the chromatin accessibility landscape. In these cells, apoptosis induced by ASCL1 co- expression involves both caspase-dependent and -independent mechanisms (right).

Article Snippet: Cell lysates were prepared and subjected to immunoblot analysis as previously described61 using antibodies against GAPDH (Santa Cruz Biotechnology, Dallas, TX), ASCL1 (24B72D11, BD Biosciences), NEUROD1 (D35G2, CST), YAP1/TAZ (D24E4, CST), YAP1 (D8H1X, CST), POU2F3 (polyclonal, Sigma-Aldrich), ATOH1 (polyclonal, Proteintech, Rosemont, IL), MYC (polyclonal, Santa Cruz Biotechnology), cleaved PARP (Asp214, CST), BCL2 (D17C4, CST), MCL1 (D35A5, CST), BCL-XL (54H6, CST), E-cadherin (24E10,CST),N-cadherin (D4R1H,CST), ZO-1 (D7D12,CST), Vimentin (D21H13, CST), Snail (C15D3, CST), Slug (C19G7, CST), phospho-histoneH2A.X (Ser139; 20E3, CST), Cyclin B1 (polyclonal, CST), and Cyclin D1 (92G2, CST).

Techniques: Expressing, Genome Wide