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aa 2 212  (R&D Systems)


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    Structured Review

    R&D Systems aa 2 212
    Aa 2 212, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+recombinant+bcl+2+proteins/Recombinant+Human+Bcl-xL+(minus+C-Terminus)+Protein%2C+CF/pmc13046825-412-21-26
    Average 94 stars, based on 5 article reviews
    aa 2 212 - by Bioz Stars, 2026-10
    94/100 stars

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    Recombinant:

    Article Title: Structures of the ApoL1 and ApoL2 N-terminal domains reveal a non-classical four-helix bundle motif
    Article Snippet: Generally, Bcl-2 proteins were immobilized on a CM5 sensor chip directly via the Amine Coupling Kit, or indirectly using the His-Capture Kit (GE Healthcare). .. Human recombinant Bcl-2 proteins were purchased from R&D Systems: Bcl-w, catalog # 824-BW-050; Bcl-x L , catalog # 894-BX-050; Bfl-1, catalog # 1160-A1-050; Bcl-2, catalog # 827-BC-050). .. His-tagged human Mcl-1 was purchased from Novus Bio (catalog # NBP2-51510).



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    Spheroids show heightened apoptotic sensitivity to extracellular Mg 2+ imbalance. ( a ) Representative Western blots of p53, <t>Bcl-2,</t> Bax, caspase-3, and cleaved caspase-3 in parental (2D) and spheroid-derived (SP; 3D) HT-29 cells cultured under control, moderate low Mg 2+ (0.4 mM; low-Mg), and moderate high Mg 2+ (2.5 mM; high-Mg) conditions. We conducted a quantitative analysis of ( b ) p53, ( c ) Bcl-2, ( d ) Bax, ( e ) caspase-3, and ( f ) cleaved caspase-3. ( g ) Mitochondrial membrane potential (ΔΨm) was measured by the red-to-green JC-1 fluorescence intensity ratio; FCCP served as a depolarization control. Data are mean ± SD (n = 5). Statistical analysis was performed using one-way ANOVA with Dunnett’s post hoc test for multiple comparisons versus control groups and unpaired Student’s t -test for comparisons between parental and SP groups under the same Mg 2+ condition. The significance levels are as follows: * p < 0.05, ** p < 0.01, *** p < 0.001 versus the control parental group. †† p < 0.01, ††† p < 0.01 versus parental cells under identical Mg 2+ conditions. ### p < 0.001 versus the control SP group.
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    Spheroids show heightened apoptotic sensitivity to extracellular Mg 2+ imbalance. ( a ) Representative Western blots of p53, <t>Bcl-2,</t> Bax, caspase-3, and cleaved caspase-3 in parental (2D) and spheroid-derived (SP; 3D) HT-29 cells cultured under control, moderate low Mg 2+ (0.4 mM; low-Mg), and moderate high Mg 2+ (2.5 mM; high-Mg) conditions. We conducted a quantitative analysis of ( b ) p53, ( c ) Bcl-2, ( d ) Bax, ( e ) caspase-3, and ( f ) cleaved caspase-3. ( g ) Mitochondrial membrane potential (ΔΨm) was measured by the red-to-green JC-1 fluorescence intensity ratio; FCCP served as a depolarization control. Data are mean ± SD (n = 5). Statistical analysis was performed using one-way ANOVA with Dunnett’s post hoc test for multiple comparisons versus control groups and unpaired Student’s t -test for comparisons between parental and SP groups under the same Mg 2+ condition. The significance levels are as follows: * p < 0.05, ** p < 0.01, *** p < 0.001 versus the control parental group. †† p < 0.01, ††† p < 0.01 versus parental cells under identical Mg 2+ conditions. ### p < 0.001 versus the control SP group.
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    Downregulation of REDD1 promotes A549 and H1299 cell apoptosis under hypoxia. ( A , B ) Apoptosis of A549 and H1299 cells following the knockdown of REDD1 was detected by flow cytometric analysis of Annexin V-FITC/PI. ( C , D ) Quantitation of apoptotic cells. ( E , F ) Protein expression of Bax and <t>Bcl2</t> was determined by Western blot. n = 4. * p < 0.05; ** p < 0.01.
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    Image Search Results


    Spheroids show heightened apoptotic sensitivity to extracellular Mg 2+ imbalance. ( a ) Representative Western blots of p53, Bcl-2, Bax, caspase-3, and cleaved caspase-3 in parental (2D) and spheroid-derived (SP; 3D) HT-29 cells cultured under control, moderate low Mg 2+ (0.4 mM; low-Mg), and moderate high Mg 2+ (2.5 mM; high-Mg) conditions. We conducted a quantitative analysis of ( b ) p53, ( c ) Bcl-2, ( d ) Bax, ( e ) caspase-3, and ( f ) cleaved caspase-3. ( g ) Mitochondrial membrane potential (ΔΨm) was measured by the red-to-green JC-1 fluorescence intensity ratio; FCCP served as a depolarization control. Data are mean ± SD (n = 5). Statistical analysis was performed using one-way ANOVA with Dunnett’s post hoc test for multiple comparisons versus control groups and unpaired Student’s t -test for comparisons between parental and SP groups under the same Mg 2+ condition. The significance levels are as follows: * p < 0.05, ** p < 0.01, *** p < 0.001 versus the control parental group. †† p < 0.01, ††† p < 0.01 versus parental cells under identical Mg 2+ conditions. ### p < 0.001 versus the control SP group.

    Journal: International Journal of Molecular Sciences

    Article Title: Altered Magnesium Environments Restrict Colorectal HT-29 Spheroid Growth by Disturbing Cellular Mg 2+ Homeostasis

    doi: 10.3390/ijms27020834

    Figure Lengend Snippet: Spheroids show heightened apoptotic sensitivity to extracellular Mg 2+ imbalance. ( a ) Representative Western blots of p53, Bcl-2, Bax, caspase-3, and cleaved caspase-3 in parental (2D) and spheroid-derived (SP; 3D) HT-29 cells cultured under control, moderate low Mg 2+ (0.4 mM; low-Mg), and moderate high Mg 2+ (2.5 mM; high-Mg) conditions. We conducted a quantitative analysis of ( b ) p53, ( c ) Bcl-2, ( d ) Bax, ( e ) caspase-3, and ( f ) cleaved caspase-3. ( g ) Mitochondrial membrane potential (ΔΨm) was measured by the red-to-green JC-1 fluorescence intensity ratio; FCCP served as a depolarization control. Data are mean ± SD (n = 5). Statistical analysis was performed using one-way ANOVA with Dunnett’s post hoc test for multiple comparisons versus control groups and unpaired Student’s t -test for comparisons between parental and SP groups under the same Mg 2+ condition. The significance levels are as follows: * p < 0.05, ** p < 0.01, *** p < 0.001 versus the control parental group. †† p < 0.01, ††† p < 0.01 versus parental cells under identical Mg 2+ conditions. ### p < 0.001 versus the control SP group.

    Article Snippet: Membranes were probed with specific primary antibodies against p53 (PB9008; Bosterbio, Pleasanton, CA, USA), BCL-2 (A00040; Bosterbio), Bax (A00183; Bosterbio), caspase-3 (PB9188; Bosterbio), cleaved caspase-3 (ab32042; Abcam), pS556 ULK1 (ab203207; Abcam), p62/SQSTM1 (ab109012; Abcam), TRPM6 (0ST00108W; Thermo Fisher Scientific Inc.), TRPM7 (ab729; Abcam), MagT1 (ab244490; Abcam), CNNM4 (ab191207; Abcam), Mrs2 (ab246915; Abcam), β-actin (ab6276; Abcam), and Na + /K + -ATpase (ab76020; Abcam).

    Techniques: Western Blot, Derivative Assay, Cell Culture, Control, Membrane, Fluorescence

    A unified model of Mg 2+ -dependent fate determination in colorectal cancer spheroids. This schematic summarizes the divergent cellular and metabolic outcomes in HT-29 spheroids cultured under varying extracellular Mg 2+ concentrations. Under physiological control conditions (1.0 mM Mg 2+ ), intact TRPM6/7 heterodimers sustain Mg 2+ influx, ensuring adequate cellular and mitochondrial Mg 2+ content, maintained ΔΨm, and enhanced expression of anti-apoptotic (Bcl-2) and mitochondrial Mg 2+ -import (Mrs2) proteins. Together, these processes support spheroid integrity, growth, and survival. Both low (0.4 mM) and high (2.5 mM) extracellular Mg 2+ environments disrupt Mg 2+ homeostasis through distinct initial mechanisms that converge on a common pathogenic endpoint: Mg 2+ influx collapse, mitochondrial Mg 2+ deficiency, loss of ΔΨm, and downregulation of Bcl-2 and Mrs2. These changes trigger upregulation of pro-apoptotic (Bax) and autophagic (p62) markers, leading to increased apoptosis and autophagy, ultimately resulting in spheroid disintegration. The model underscores the dual vulnerability of colorectal cancer spheroids to Mg 2+ dysregulation and highlights the TRPM6/7–Mrs2 axis as a central node for therapeutic intervention.

    Journal: International Journal of Molecular Sciences

    Article Title: Altered Magnesium Environments Restrict Colorectal HT-29 Spheroid Growth by Disturbing Cellular Mg 2+ Homeostasis

    doi: 10.3390/ijms27020834

    Figure Lengend Snippet: A unified model of Mg 2+ -dependent fate determination in colorectal cancer spheroids. This schematic summarizes the divergent cellular and metabolic outcomes in HT-29 spheroids cultured under varying extracellular Mg 2+ concentrations. Under physiological control conditions (1.0 mM Mg 2+ ), intact TRPM6/7 heterodimers sustain Mg 2+ influx, ensuring adequate cellular and mitochondrial Mg 2+ content, maintained ΔΨm, and enhanced expression of anti-apoptotic (Bcl-2) and mitochondrial Mg 2+ -import (Mrs2) proteins. Together, these processes support spheroid integrity, growth, and survival. Both low (0.4 mM) and high (2.5 mM) extracellular Mg 2+ environments disrupt Mg 2+ homeostasis through distinct initial mechanisms that converge on a common pathogenic endpoint: Mg 2+ influx collapse, mitochondrial Mg 2+ deficiency, loss of ΔΨm, and downregulation of Bcl-2 and Mrs2. These changes trigger upregulation of pro-apoptotic (Bax) and autophagic (p62) markers, leading to increased apoptosis and autophagy, ultimately resulting in spheroid disintegration. The model underscores the dual vulnerability of colorectal cancer spheroids to Mg 2+ dysregulation and highlights the TRPM6/7–Mrs2 axis as a central node for therapeutic intervention.

    Article Snippet: Membranes were probed with specific primary antibodies against p53 (PB9008; Bosterbio, Pleasanton, CA, USA), BCL-2 (A00040; Bosterbio), Bax (A00183; Bosterbio), caspase-3 (PB9188; Bosterbio), cleaved caspase-3 (ab32042; Abcam), pS556 ULK1 (ab203207; Abcam), p62/SQSTM1 (ab109012; Abcam), TRPM6 (0ST00108W; Thermo Fisher Scientific Inc.), TRPM7 (ab729; Abcam), MagT1 (ab244490; Abcam), CNNM4 (ab191207; Abcam), Mrs2 (ab246915; Abcam), β-actin (ab6276; Abcam), and Na + /K + -ATpase (ab76020; Abcam).

    Techniques: Cell Culture, Control, Expressing

    Downregulation of REDD1 promotes A549 and H1299 cell apoptosis under hypoxia. ( A , B ) Apoptosis of A549 and H1299 cells following the knockdown of REDD1 was detected by flow cytometric analysis of Annexin V-FITC/PI. ( C , D ) Quantitation of apoptotic cells. ( E , F ) Protein expression of Bax and Bcl2 was determined by Western blot. n = 4. * p < 0.05; ** p < 0.01.

    Journal: Biomedicines

    Article Title: REDD1 Affects Proliferation, Apoptosis, Migration, and Colony Formation via p-ERK and p-JNK Signaling in Lung Adenocarcinoma Cells Under Hypoxia

    doi: 10.3390/biomedicines13122918

    Figure Lengend Snippet: Downregulation of REDD1 promotes A549 and H1299 cell apoptosis under hypoxia. ( A , B ) Apoptosis of A549 and H1299 cells following the knockdown of REDD1 was detected by flow cytometric analysis of Annexin V-FITC/PI. ( C , D ) Quantitation of apoptotic cells. ( E , F ) Protein expression of Bax and Bcl2 was determined by Western blot. n = 4. * p < 0.05; ** p < 0.01.

    Article Snippet: B-cell lymphoma-2 (Bcl2) (A00040-1) antibody was obtained from Boster (Wuhan, China). p-p44/42 MAPK (ERK1/2) (Thr202/Tyr204) (#9101), p44/42 MAPK (ERK1/2) (#4695), p-SAPK/JNK (Thr183/Tyr185) (#4668), SAPK/JNK (#9252), p-p38 MAPK (Thr180/Tyr182) (#9211), p38 mitogen-activated protein kinase (MAPK) (#9212), p-Akt (Ser473), Akt (#9271), p-mTOR (Ser2448) (#5536), and mTOR antibodies (#2974) were acquired from Cell Signaling Technology Inc. (Beverly, MA, USA), while the β-actin (DKM9001L) antibody was obtained from Sungene Biotech Co., Ltd. (Tianjin, China).

    Techniques: Knockdown, Quantitation Assay, Expressing, Western Blot