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Proteintech nfκb2
Nfκb2, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nf%CE%BAb2/10__1172_slash_jci192074-440-92-94?v=Proteintech
Average 93 stars, based on 11 article reviews

nfκb2 - by Bioz Stars, 2026-07

93/100 stars

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Mitochondria (ATP synthase, Complex V)-targeted therapy sensitized blasts to TKI treatments but nuclear genomes of blasts underwent reprogramming to survive. (N = 3). ( A ) Representative FC plots of different experimental groups with NO TX, 80 nM gilteritinib (GILT), 100 nM oligomycin (OA), and GILT + OA on viability dye and CD44 expression; Red circle indicates CD44+/viability dye- (negative) viable blasts; Right table: Cumulative percentage data of viable CD44+ cells in different treatment groups; ( B ) Gene expression of GDF15 , a biomarker for mitochondrial diseases or oxidative stress, was analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of GDF15 in different treatment groups; ( C ) Gene expression of NRF1 (nuclear respiratory factor 1), a key transcription regulator of mitochondrial biogenesis, was analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NRF1 in different treatment groups; ( D ) Representative FC histograms showing expression of NRF1 in viable MV4-11 cells that had IgG-staining control (orange plot line); NO TX (gray plot line); 100 nM oligomycin (OA)-treated experimental groups (red plot line); Right table: Cumulative MFI (mean fluorescence intensity) data of NRF1 + viable cells of different treatment groups; ( E ) Gene expressions of NFκB1 and NFκB2 , transcription factors that rapidly respond to cellular stimuli, were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NFκB1 and NFκB2 in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: Mitochondria (ATP synthase, Complex V)-targeted therapy sensitized blasts to TKI treatments but nuclear genomes of blasts underwent reprogramming to survive. (N = 3). ( A ) Representative FC plots of different experimental groups with NO TX, 80 nM gilteritinib (GILT), 100 nM oligomycin (OA), and GILT + OA on viability dye and CD44 expression; Red circle indicates CD44+/viability dye- (negative) viable blasts; Right table: Cumulative percentage data of viable CD44+ cells in different treatment groups; ( B ) Gene expression of GDF15 , a biomarker for mitochondrial diseases or oxidative stress, was analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of GDF15 in different treatment groups; ( C ) Gene expression of NRF1 (nuclear respiratory factor 1), a key transcription regulator of mitochondrial biogenesis, was analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NRF1 in different treatment groups; ( D ) Representative FC histograms showing expression of NRF1 in viable MV4-11 cells that had IgG-staining control (orange plot line); NO TX (gray plot line); 100 nM oligomycin (OA)-treated experimental groups (red plot line); Right table: Cumulative MFI (mean fluorescence intensity) data of NRF1 + viable cells of different treatment groups; ( E ) Gene expressions of NFκB1 and NFκB2 , transcription factors that rapidly respond to cellular stimuli, were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NFκB1 and NFκB2 in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Article Snippet: The lentiviral transfer plasmids ( ) contain a full-length open reading frame (ORF) of human NFκB2 (GeneCopoeia catalog#: EX-Z4293-Lv225, Rockville, MD, USA), NFκB1 (GeneCopoeia catalog#: EX-F0208-Lv224), RELB (GeneCopoeia catalog#: EX-G0029-Lv224), and NFκB2-RELB bicistronic plasmid (custom-built by GeneCopoeia with catalog#: CS-Z4293-Lv225-01).

Techniques: Expressing, Biomarker Assay, Staining, Control, Fluorescence

New transgenic cell lines of NFκB -family genes reveal that NFκB2 overexpression (OE) promotes gene expressions of TFAM, TFB2M and NRF1 in vitro. (N = 3). ( A ) Schematic diagram of lentiviral expression constructs containing open-reading frames (ORF) of human NFκB2, RELB , or NFκB1 genes and eGFP or mCherry reporters, with promoters EF1a and IRES2, respectively; A bicistronic lenti-plasmid expresses both NFκB2 and RELB controlled by EF1a and IRES promoters, respectively; Six new transgenic cell lines overexpressing NFκB family transgenes in leukemia blast MV4-11 were generated, including: NFκB2 - eGFP -MV411, NFκB1-mCherry -MV411, RELB - mCherry -MV411, NFκB2 - RELB - eGFP -MV411, NFκB2 -eGFP/ RELB-mCherry -MV411, NFκB2 -eGFP/ NFKB1-mCherry -MV411; and GFP -MV411 will be the vector control without transgene ORF insert; ( B ) All new cell lines were purified by FACS-sorting (see Materials and Methods); A representative FC plot shows multiple populations with eGFP and/or mCherry expression which were identified as NFκB2 - eGFP -MV411, RELB - mCherry -MV411, NFκB2-eGFP/RELB-mCherry -MV411 before purification; ( C ) Gene expressions of NFκB2, NRF1, TFAM and TFB2M were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of genes; ( D ) Representative FC plots show protein expressions of TFAM and/or TFB2M in NFκB2-eGFP -MV411 and GFP -MV411 (vector control); Right table: Cumulative percentage data of viable TFAM+/TFB2M+ cells in different groups; ( E ) Gene expressions of NFκB2 and TFAM after shRNA knockdown of NFκB2 in MV4-11 cells, analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NFκB2 and TFAM in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: New transgenic cell lines of NFκB -family genes reveal that NFκB2 overexpression (OE) promotes gene expressions of TFAM, TFB2M and NRF1 in vitro. (N = 3). ( A ) Schematic diagram of lentiviral expression constructs containing open-reading frames (ORF) of human NFκB2, RELB , or NFκB1 genes and eGFP or mCherry reporters, with promoters EF1a and IRES2, respectively; A bicistronic lenti-plasmid expresses both NFκB2 and RELB controlled by EF1a and IRES promoters, respectively; Six new transgenic cell lines overexpressing NFκB family transgenes in leukemia blast MV4-11 were generated, including: NFκB2 - eGFP -MV411, NFκB1-mCherry -MV411, RELB - mCherry -MV411, NFκB2 - RELB - eGFP -MV411, NFκB2 -eGFP/ RELB-mCherry -MV411, NFκB2 -eGFP/ NFKB1-mCherry -MV411; and GFP -MV411 will be the vector control without transgene ORF insert; ( B ) All new cell lines were purified by FACS-sorting (see Materials and Methods); A representative FC plot shows multiple populations with eGFP and/or mCherry expression which were identified as NFκB2 - eGFP -MV411, RELB - mCherry -MV411, NFκB2-eGFP/RELB-mCherry -MV411 before purification; ( C ) Gene expressions of NFκB2, NRF1, TFAM and TFB2M were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of genes; ( D ) Representative FC plots show protein expressions of TFAM and/or TFB2M in NFκB2-eGFP -MV411 and GFP -MV411 (vector control); Right table: Cumulative percentage data of viable TFAM+/TFB2M+ cells in different groups; ( E ) Gene expressions of NFκB2 and TFAM after shRNA knockdown of NFκB2 in MV4-11 cells, analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of NFκB2 and TFAM in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Techniques: Transgenic Assay, Over Expression, In Vitro, Expressing, Construct, Plasmid Preparation, Generated, Control, Purification, shRNA, Knockdown

Visualization of mitochondrial NFκB2 in MV4-11 blasts. ( N = 3 ) . ( A ) Generation of P100-eGFP (fusion)-MV4-11 cell line through the lentiviral system; Consistent with P100-eGFP (fusion)-HEK-293T cells, P100-eGFP was localized in cytoplasm of MV4-11. The immunocytochemistry (representative fluorescent images) was performed to show the co-localization of MitoView™633-stained mitochondria and GFP+ mitochondria at low magnification with a scale bar of 10 µm. ( B , C ) The white box of ( A ) was magnified to show many GFP+ mitochondria by a GFP-fluorescent image (indicated by white arrows, ( B ) and by a Phase-bright image of mitochondrial morphology (indicated by black arrows, ( C ) in these P100-eGFP (fusion)-MV4-11 cells with a scale bar of 20 µm.

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: Visualization of mitochondrial NFκB2 in MV4-11 blasts. ( N = 3 ) . ( A ) Generation of P100-eGFP (fusion)-MV4-11 cell line through the lentiviral system; Consistent with P100-eGFP (fusion)-HEK-293T cells, P100-eGFP was localized in cytoplasm of MV4-11. The immunocytochemistry (representative fluorescent images) was performed to show the co-localization of MitoView™633-stained mitochondria and GFP+ mitochondria at low magnification with a scale bar of 10 µm. ( B , C ) The white box of ( A ) was magnified to show many GFP+ mitochondria by a GFP-fluorescent image (indicated by white arrows, ( B ) and by a Phase-bright image of mitochondrial morphology (indicated by black arrows, ( C ) in these P100-eGFP (fusion)-MV4-11 cells with a scale bar of 20 µm.

Techniques: Immunocytochemistry, Staining

NFκB2 activated promoters of dual mitochondrial-nuclear genomes in vitro. ( N = 3 ) . ( A ) Sequence information of lentiviral vector constructs (custom-built by GeneCopoeia) of mitochondrial LSP promoter (blue sequence), HSP1 promoter (red sequence) or HSP1/HSP2 promoter (underlined sequence) and a NFκB2-binding sequence (green sequence and named as Enhancer); ( B , C ) Promoter assays of mitochondrial genome ( B ) and nuclear genome ( C ) in blasts were performed (see details in the Materials and Methods); representative live images show luciferase activity in the supernatants of different experimental groups; ( D ) A schematic diagram illustrating the NFκB2-binding sequence on the D-loop of human mitochondrial DNA genome; Under pathologic or physiologic condition, NFκB2 may activate mitochondrial LSP promoter, HSP1/2 promoters and nuclear TFAM promoter to initiate mitochondrial biogenesis.

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: NFκB2 activated promoters of dual mitochondrial-nuclear genomes in vitro. ( N = 3 ) . ( A ) Sequence information of lentiviral vector constructs (custom-built by GeneCopoeia) of mitochondrial LSP promoter (blue sequence), HSP1 promoter (red sequence) or HSP1/HSP2 promoter (underlined sequence) and a NFκB2-binding sequence (green sequence and named as Enhancer); ( B , C ) Promoter assays of mitochondrial genome ( B ) and nuclear genome ( C ) in blasts were performed (see details in the Materials and Methods); representative live images show luciferase activity in the supernatants of different experimental groups; ( D ) A schematic diagram illustrating the NFκB2-binding sequence on the D-loop of human mitochondrial DNA genome; Under pathologic or physiologic condition, NFκB2 may activate mitochondrial LSP promoter, HSP1/2 promoters and nuclear TFAM promoter to initiate mitochondrial biogenesis.

Techniques: In Vitro, Sequencing, Plasmid Preparation, Construct, Binding Assay, Luciferase, Activity Assay

Novel therapies eliminated AML blasts in vitro by inhibiting their mitochondrial biogenesis and functions. ( N = 3 ). ( A ) Representative FC plots of different experimental groups of MV4-11 cells with NO TX, 80 nM GILT, 100 nM oligomycin (OA), 15 µM SN52 (NFκB2-I), or 15 µM BAY11-7082 (NFκB-I), GILT + OA, GILT + SN52, GILT + SN52 + OA and GILT + SN52 + OA + BAY, which were analyzed by cell death biomarkers including Annexin-V (apoptosis), Propidium Iodide (PI, necrosis) and Annexin-V+/PI+ (dead); The blue arrows indicate Annexin-V+/PI- cells (early apoptotic); The orange arrows indicate Annexin-V+/PI+ cells (late-stage dying or dead cells); ( B ) Upper panel: Cumulative percentage data of viable MV4-11 blasts in different treatment groups (both Annexin-V negative /PI negative populations in the FC plots); Lower panel: Cumulative percentage data of Annexin-V+/PI- cells (blue column and indicated by blue arrows in plots of ( A )), and Annexin-V+/PI+ cells (orange column and indicated by orange arrows in plots of ( A )) in different treatment groups; ( C ) Gene expressions of TFAM were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of TFAM in different treatment groups; ( D ) ATP concentration was measured in MV411 cells of different treatment groups; ( E ) Representative FC histograms show expression of MitoView™633 in different treatment groups with NO TX, GILT + SN52 + OA and GILT + SN52 + BAY + OA; Right table: Cumulative MFI (mean fluorescence intensity) data of MitoView™633 expression in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: Novel therapies eliminated AML blasts in vitro by inhibiting their mitochondrial biogenesis and functions. ( N = 3 ). ( A ) Representative FC plots of different experimental groups of MV4-11 cells with NO TX, 80 nM GILT, 100 nM oligomycin (OA), 15 µM SN52 (NFκB2-I), or 15 µM BAY11-7082 (NFκB-I), GILT + OA, GILT + SN52, GILT + SN52 + OA and GILT + SN52 + OA + BAY, which were analyzed by cell death biomarkers including Annexin-V (apoptosis), Propidium Iodide (PI, necrosis) and Annexin-V+/PI+ (dead); The blue arrows indicate Annexin-V+/PI- cells (early apoptotic); The orange arrows indicate Annexin-V+/PI+ cells (late-stage dying or dead cells); ( B ) Upper panel: Cumulative percentage data of viable MV4-11 blasts in different treatment groups (both Annexin-V negative /PI negative populations in the FC plots); Lower panel: Cumulative percentage data of Annexin-V+/PI- cells (blue column and indicated by blue arrows in plots of ( A )), and Annexin-V+/PI+ cells (orange column and indicated by orange arrows in plots of ( A )) in different treatment groups; ( C ) Gene expressions of TFAM were analyzed by qPCR. Data of mRNA expressions show the fold change (normalized to β-actin ) of TFAM in different treatment groups; ( D ) ATP concentration was measured in MV411 cells of different treatment groups; ( E ) Representative FC histograms show expression of MitoView™633 in different treatment groups with NO TX, GILT + SN52 + OA and GILT + SN52 + BAY + OA; Right table: Cumulative MFI (mean fluorescence intensity) data of MitoView™633 expression in different treatment groups; Where applicable, data are means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.005.

Techniques: In Vitro, Concentration Assay, Expressing, Fluorescence

$Overview of inhibiting NFκB2-mediated mitochondrial-nuclear transcriptional adaptation to overcome AML relapse. ( A ) Mitochondria-targeted drugs such as oligomycin, an ATP synthase blocker (Complex V) can improve the therapeutic efficacy of TKIs; however, mitochondrial damage and stress result in the activation of pro-survival transcription factors of noncanonical NFκB2 in refractory blasts. ( B ) Notably, increased NFκB2 can promote the nuclear gene (nDNA) expression of TFAM , TFB2M , and NRF1 , which are known to be essential for mitochondrial biogenesis and metabolic plasticity, in addition to its activation of a group of pro-inflammatory and pro-survival factors such as CD44/cytokines/receptors (as we reported previously), thus leading to a large cascading effect on homeostatic adaptation to support blast survival and AML relapse energetically and metabolically. Increased NFKB2 enters the mitochondria and binds specific “TTGGGGGGTG” region of D-loop to promote biogenesis and biosynthesis to support the respiratory chain for ATP/metabolites production. ( C ) In this regard, we developed a novel triplet strategy blocking FLT3 signaling, targeting blast mitochondrial energy conversion, and inhibiting NFκB2 simultaneously, which can effectively promote the terminal death of AML blasts and prevent AML relapse.$

Journal: International Journal of Molecular Sciences

Article Title: Discovery of NFκB2-Coordinated Dual Regulation of Mitochondrial and Nuclear Genomes Leads to an Effective Therapy for Acute Myeloid Leukemia

doi: 10.3390/ijms25158532

Figure Lengend Snippet: Overview of inhibiting NFκB2-mediated mitochondrial-nuclear transcriptional adaptation to overcome AML relapse. ( A ) Mitochondria-targeted drugs such as oligomycin, an ATP synthase blocker (Complex V) can improve the therapeutic efficacy of TKIs; however, mitochondrial damage and stress result in the activation of pro-survival transcription factors of noncanonical NFκB2 in refractory blasts. ( B ) Notably, increased NFκB2 can promote the nuclear gene (nDNA) expression of TFAM , TFB2M , and NRF1 , which are known to be essential for mitochondrial biogenesis and metabolic plasticity, in addition to its activation of a group of pro-inflammatory and pro-survival factors such as CD44/cytokines/receptors (as we reported previously), thus leading to a large cascading effect on homeostatic adaptation to support blast survival and AML relapse energetically and metabolically. Increased NFKB2 enters the mitochondria and binds specific “TTGGGGGGTG” region of D-loop to promote biogenesis and biosynthesis to support the respiratory chain for ATP/metabolites production. ( C ) In this regard, we developed a novel triplet strategy blocking FLT3 signaling, targeting blast mitochondrial energy conversion, and inhibiting NFκB2 simultaneously, which can effectively promote the terminal death of AML blasts and prevent AML relapse.

Techniques: Activation Assay, Expressing, Metabolic Labelling, Blocking Assay

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