- MA1-06101 - Invitrogen Antibodies LMNA antibody

Submitted references Vascular senescence in progeria: role of endothelial dysfunction.

Xu Q, Mojiri A, Boulahouache L, Morales E, Walther BK, Cooke JP
European heart journal open 2022 Jul;2(4):oeac047

Mechanical phenotyping reveals unique biomechanical responses in retinoic acid-resistant acute promyelocytic leukemia.

Li B, Maslan A, Kitayama SE, Pierce C, Streets AM, Sohn LL
iScience 2022 Feb 18;25(2):103772

Apico-basal cell compression regulates Lamin A/C levels in epithelial tissues.

Iyer KV, Taubenberger A, Zeidan SA, Dye NA, Eaton S, Jülicher F
Nature communications 2021 Mar 25;12(1):1756

Dysfunction of iPSC-derived endothelial cells in human Hutchinson-Gilford progeria syndrome.

Matrone G, Thandavarayan RA, Walther BK, Meng S, Mojiri A, Cooke JP
Cell cycle (Georgetown, Tex.) 2019 Oct;18(19):2495-2508

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot analysis was performed on nuclear enriched cell extracts (30 µg lysate) of HeLa (Lane 1), A-431 (Lane 2), HEK293T (Lane 3), U-2 OS (Lane 4), Jurkat (Lane 5) and HL-60 (Lane 6). The blot was probed with Anti- Lamin A Antibody (Product # MA1-06101, 1µg/mL) and detected by chemiluminescence using Goat anti-Mouse IgG (H+L) Superclonal™ Secondary Antibody, HRP conjugate (Product # A28177, 0.25 µg/mL, 1:4000 dilution). A 74 kDa band corresponding to Lamin A was observed across all the cell lines tested except Jurkat and HL-60.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: CRISPR-Cas9 mediated genome editing ofLamin A (as confirmed by next generation sequencing) was achieved by using LentiArray™ Lentiviral sgRNA (Product # A32042, Assay ID CRISPR817702_LV) and LentiArray Cas9 Lentivirus (Product # A32064). Fig (a) Western blot analysis of Lamin A was performed by loading 30 µg of HeLa wild type (Lane 1), HeLa Cas9 (Lane 2) and HeLa Cas9 cells transduced with Lamin A Lentiviral sgRNA (Lane 3) modified whole cell extracts. The samples were electrophoresed using NuPAGE™ Novex™ 4-12% Bis-Tris Protein Gel (Product # NP0322BOX). Resolved proteins were then transferred onto a nitrocellulose membrane (Product # IB23001) by iBlot® 2 Dry Blotting System (Product # IB21001). The blot was probed with Anti-Lamin A Monoclonal Antibody (133A2) (Product # MA1-06101) using 1 µg/mL dilution and Goat anti-Mouse IgG (H+L) Superclonal™ Recombinant Secondary Antibody, HRP (Product # A28177 1:5000 dilution).Chemiluminescent detection was performed using Novex® ECL Chemiluminescent Substrate Reagent Kit (Product # WP20005). A reduced signal in sgRNA transduced cells using the LentiArray™ CRISPR product line confirms that antibody is specific toLamin A (Fig (b)).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunocytochemical staining of fiboblasts showing nuclear lamina stained with Lamin A monoclonal antibody (Product # MA1-06101).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunocytochemical staining of fiboblasts showing nuclear lamina stained with Lamin A monoclonal antibody (Product # MA1-06101).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunofluorescence analysis of Lamin A was performed using 70% confluent log phase HeLa cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 10 minutes, and blocked with 1% BSA for 1 hour at room temperature. The cells were labeled with Lamin A Monoclonal Antibody (133A2) (Product # MA1-06101) at 5 µg/mL in 0.1% BSA and incubated overnight at 4 degree and then labeled with Goat anti-Mouse IgG (H+L) Superclonal™ Secondary Antibody, Alexa Fluor® 488 conjugate (Product # A28175) at a dilution of 1:2000 for 45 minutes at room temperature (Panel a: green). Nuclei (Panel b: blue) were stained with SlowFade® Diamond Antifade Mountant with DAPI (Product # P36962). F-actin (Panel c: red) was stained with Rhodamine Phalloidin (Product # R415, 1:300). Panel d represents the merged image showing nuclear membrane localization. Panel e shows the no primary antibody control. The images were captured at 60X magnification.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry on frozen sections of human colon showing nuclear lamina staining in epithelial and connective tissue cells stained with Lamin A monoclonal antibody (Product # MA1-06101).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry on paraffin section of human colon stained with Lamin A monoclonal antibody (Product # MA1-06101).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Chromatin Immunoprecipitation-Western Blot (ChIP-WB) of endogenous Lamin A protein using Anti-Lamin A Antibody: ChIP was performed using Lamin A Mouse Monoclonal Antibody (Product # MA1-06101, 10 µg) (lane 2) on sheared chromatin from 4 million formaldehyde fixed HeLa cells. Normal Rabbit IgG (lane 1) was used as negative IP control. Western blot analysis of immunoprecipitated proteins was performed using Lamin A/C Mouse Monoclonal Antibody (Product # MA1-5820, 1:200 dilution).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 6 Regulation of Lamin A/C by apico-basal cell compression is also observed in mammalian epithelial cells. a Image showing high-density culture of 5700 cells/mm 2 . Tight junction protein ZO-1 is shown in magenta, Lamin A in green, and DAPI in blue. Scalebar, 15 um. b Enlarged images of the region shown by the orange ROI in ( h ). DAPI is shown in blue and Lamin A is shown in color-coded intensity. Scale bar, 10 um. c Image showing low density culture of 70 cells/ mm 2 . Tight junction protein ZO-1 is shown in magenta, Lamin A in green, and DAPI in blue. Scalebar, 15 um. d Enlarged images of the region shown by orange ROI in ( j ). DAPI is shown in blue, and Lamin A is shown in color-coded intensity. Scale bar, 10 um. e Binned scatter plot between D cell and D nuc generated by binning D cell in bins of 0.07. Each point in the plot represents mean value of D cell and D nuc in the bin. The red points represent data from HD culture and cyan points represent data from LD culture. The data are presented as mean +- S.E.M. Solid red line represents the linear regression to the data. Pearson's correlation coefficient R p is 0.97. f Box-plot showing LamA in high density (HD) and low density (LD) cultures. The sample number, n represents the number of cells analyzed over 3 independent biological replicates. g Binned scatter plot between D nuc and LamA intensity generated by binning D nuc in bins of 0.06. Each point in the plot represents mean value of D nuc and LamA in the bin. The

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Progerin causes senescence phenotype in both endothelial cells and vascular smooth muscle cells of Hutchinson-Gilford progeria syndrome. ( A ) Quantitative reverse transcription polymerase chain reaction for progerin expression in endothelial cells and vascular smooth muscle cells. n = 4 for control-ECs, and n = 3 for other groups. ( B and C ) Western blot and its quantification of progerin level in endothelial cells and vascular smooth muscle cells. n = 4. ( D ) Immunofluorescence staining of lamin A for nuclear morphology and quantification in ( E ); the white arrows represent abnormal nuclei. n = 4. ( F ) A representative figure of metaphase spread (blue: DAPI nucleus, red: cy5 telomere, scale bar: 20 mum). ( G ) Telomere probe intensities were normalized with the DAPI signal for both endothelial cells and vascular smooth muscle cells, n = 33 metaphase spread for each group, replicated at least three times. ( H ) Real-time cell proliferation using xCELLigence measured by impedance for both endothelial cells and vascular smooth muscle cells from control and Hutchinson-Gilford progeria syndrome. n = 4, replicated three times. ( I and J ) Increased beta-galactosidase staining in both HGPS-ECs and HGPS-VSMCs compared with respective controls, with an especially higher percentage in HGPS-ECs among all groups (scale bar: 300 mum) n = 5 for HGPS-ECs, n = 4 for other groups. ( K ) Quantitative reverse transcription polymerase chain reaction for P16 and P21 expression in endothelia

MA1-06101

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