|
Abnova
rabbit polyclonal anti-camk2d antibodies  Rabbit Polyclonal Anti Camk2d Antibodies, supplied by Abnova, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pmc11041739-313-31-36?v=Abnova Average 90 stars, based on 1 article reviews
rabbit polyclonal anti-camk2d antibodies - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
|
PeproTech
rabbit antihuman polyclonal antibodies against golph3  Rabbit Antihuman Polyclonal Antibodies Against Golph3, supplied by PeproTech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pmc07057801-38-5-17?v=PeproTech Average 90 stars, based on 1 article reviews
rabbit antihuman polyclonal antibodies against golph3 - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
|
WuXi AppTec
polyclonal rabbit anti-human primary antibodies against csgalnact-1  Polyclonal Rabbit Anti Human Primary Antibodies Against Csgalnact 1, supplied by WuXi AppTec, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pmc03779571-89-4-12?v=WuXi+AppTec Average 90 stars, based on 1 article reviews
polyclonal rabbit anti-human primary antibodies against csgalnact-1 - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
|
Alomone Labs
anti-human orai1 (extracellular) antibody Anti Human Orai1 (Extracellular) Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/custom%40acc-060%4025769459?v=Alomone+Labs Average 94 stars, based on 1 article reviews
anti-human orai1 (extracellular) antibody - by Bioz Stars,
2026-08
94/100 stars
|
Buy from Supplier |
|
GeneTex
rabbit anti-human polyclonal antibodies against rnakl Rabbit Anti Human Polyclonal Antibodies Against Rnakl, supplied by GeneTex, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pm29582699-47-18-26?v=GeneTex Average 90 stars, based on 1 article reviews
rabbit anti-human polyclonal antibodies against rnakl - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
|
SangStat Inc
rabbit-derived polyclonal antibody against anti-human thymocytes thymoglobulin Rabbit Derived Polyclonal Antibody Against Anti Human Thymocytes Thymoglobulin, supplied by SangStat Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pm14756271-18-1-9?v=SangStat+Inc Average 90 stars, based on 1 article reviews
rabbit-derived polyclonal antibody against anti-human thymocytes thymoglobulin - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
|
Cayman Chemical
rabbit anti-aif polyclonal antibodies against amino acids 151–180 of human aif Rabbit Anti Aif Polyclonal Antibodies Against Amino Acids 151–180 Of Human Aif, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/rabbit+polyclonal+anti-human+antibody+raised+against+nestin/pm24129923-64-9-11?v=Cayman+Chemical Average 90 stars, based on 1 article reviews
rabbit anti-aif polyclonal antibodies against amino acids 151–180 of human aif - by Bioz Stars,
2026-08
90/100 stars
|
Buy from Supplier |
Image Search Results
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Identification of BBLN in TOF patient heart specimens by nano-LC–ESI–MS/MS analysis of CAMK2D-co-enriched proteins in the 8–14 kDa range. b , AP of CAMK2D from cardiac specimens of TOF patients (AP: CAMK2D) followed by IB detection of enriched CAMK2D (IB: CAMK2D) and co-enriched BBLN (IB: BBLN). The control immunoaffinity matrix (AP: con) did not enrich CAMK2D nor BBLN. The experiment was repeated three times with similar results. c , Characteristics of TOF patients who were included in the study for the immunohistological determination of cardiac BBLN. Age between acyanotic and cyanotic TOF patients was comparable while oxygen saturation (sat.) was significantly different. d , Immunohistological detection of BBLN on cardiac specimens of TOF patients without (left) and with cyanosis (right). Scale bar, 40 μm. Immunohistological detection of BBLN was performed on specimens of 16 acyanotic TOF patients and 16 cyanotic TOF patients (cf. f and g ). e – g , Immunohistological determination of BBLN on cardiac specimens of 16 acyanotic TOF patients – and 16 cyanotic TOF patients – . Counterstaining was performed with hematoxylin (HE). Quantitative BBLN data ( e ) and immunohistological images of cardiac specimens from acyanotic TOF patients ( f ) and cyanotic TOF patients ( g ) are shown. Scale bar, 2 mm. Data are mean ± s.d. ( n = 16 patients per group; unpaired, two-tailed t -test; d.f. 30; c , t = 2.010 and 7.820, P = 0.05354 and 9.99913 × 10 −9 ; e , t = 7.811 and P = 1.02375 × 10 −8 ).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Tandem Mass Spectroscopy, Control, Two Tailed Test
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Immunofluorescence colocalization of BBLN with CAMK2D on a heart specimen of an 8-month-old, male Tg- BBLN mouse (scale bar, 40 μm). The immunofluorescence colocalization was performed with heart specimens of five different Tg- BBLN mice (Tg-1) and five different nontransgenic FVB controls. All immunofluorescence images are shown in Supplementary Fig. . b , Quantitative IB determination of cardiac contents of activated phospho-T287–CAMK2D, inactive phospho-T307–CAMK2D, total CAMK2D and BBLN in 8-month-old, Tg- BBLN mice (Tg-1) and age- and sex-matched nontransgenic FVB control mice. The lower control IB detects ATP5A1. Left: IB images and right: quantitative IB data (mean ± s.d., n = 9 mice per group, 5 males and 4 females; unpaired, two-tailed t -test; d.f. 16, t = 32.92, 8.467, 2.602 and 56.01; P = 3.9625 × 10 −16 , 2.63699 × 10 −7 , 0.01927 and 8.64361 × 10 −20 ). c , d , In vitro data show that recombinant BBLN protein enhanced the autophosphorylation of recombinant CAMK2D (200 nM) and the CAMK2D-mediated substrate phosphorylation of recombinant PDC and BBLN. Representative autoradiography images ( c ) and quantitative data ( d ) of BBLN-enhanced PDC phosphorylation by CAMK2D (50 nM) in vitro, in the presence and absence (w/o) of Ca 2+ +calmodulin (CALM) (mean ± s.d., n = 3 biological replicates, one-way ANOVA and Dunnett’s test; F (9,20) = 38.33; P = 0.9998, 0.3728, <0.0001 and <0.0001 BBLN+Ca 2+ +CALM versus Cont.+Ca 2+ +CALM; ** P = 0.0052 versus Cont.+Ca 2+ +CALM; * P = 0.0182, 0.0321, 0.0113 and 0.0135 versus Cont.+Ca 2+ +CALM). e , Quantitative IB determination of cardiac contents of phospho-T287–CAMK2D, total CAMK2D, phospho-S2813–RYR2 and BBLN (and BBLN–SxxA) in 8-month-old, male Tg- BBLN mice (Tg-2), nontransgenic FVB mice and Tg- BBLN mice (Tg-2) after 4 weeks of lentiviral transduction of miCamk2d (Tg- BBLN +miCamk2d) and Tg- BBLN –SxxA mice. The control IB detects ATP5A1. Quantitative data (left) and IB images (right) (mean ± s.d.; n = 4 male, 8-month-old mice per group, one-way ANOVA and Tukey’s test; F (3,12) = 111.4, 27.29, 62.58 and 52.25; upper left: P = 1.914 × 10 −7 , 5.873 × 10 −9 and 3.424 × 10 −8 ; lower left: P = 0.4303, 0.00001428 and 0.5147; upper right: P = 0.000007374, 8.287 × 10 −8 and 0.000004093; lower right: P = 0.0001016, 0.0933 and 0.001294); f , The left ventricular EF and the LVIDd of 8-month-old, male mice were determined by echocardiography (mean ± s.d., n = 6 mice per group, one-way ANOVA and Tukey’s test; F (3,20) = 54.28 and 5.562; P = 1.19 × 10 −9 , 3.58 × 10 −8 , 6.628 × 10 −8 EF; P = 0.004012, 0.1793 and 0.0449 LVIDd).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Immunofluorescence, Control, Two Tailed Test, In Vitro, Recombinant, Autoradiography, Transduction
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , e Cardiac transcript levels of different Camk2d splice variants were determined by NGS in right ( a ) and left ventricles ( e ) of 3–4-month-old, male non-transgenic FVB mice and transgenic Tg- BBLN mice (Tg-1), and are presented as TPM (transcripts per million). b - d , f-h , Transcript levels of cardiac Camk2a , Camk2b and Camk2g were determined by NGS in right ventricular ( b-d ) and left ventricular heart specimens ( f-h) of non-transgenic FVB mice and transgenic Tg- BBLN mice. Data are mean ± s.d. P-values were determined by the unpaired, two-tailed t-test; just alpha; n = 4 mice per group (df=6; a , t = 2.103, 2.494, 4.952, 1.473; p = 0.0801, 0.0469, 0.0026, 0.1913; b , t = 6.433; p = 0.0007; c , t = 13.39; p = 1.0757e-05; d , t = 1.727; p = 0.1349; e , t = 3.453, 0.5919, 4.256, 1.050; p = 0.0136, 0.5755, 0.0053, 0.3342; f , 5.857; p = 0.0011; g , 4.797; p = 0.0030; h , 0.1269; p = 0.9032).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Transgenic Assay, Two Tailed Test
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Immunoblot analysis detected reduced total cardiac RYR2 protein contents and increased CAMK2D-mediated phosphorylation of RYR2 on serine-2813 in Tg- BBLN mice (Tg-1) compared to non-transgenic FVB controls. Representative immunoblots (left panels), and quantitative immunoblot data (right panels) are shown. b , Cardiac ATP2A2 (SERCA2) levels are decreased in Tg- BBLN (Tg-1) hearts. The lower control blot detects ATP5A1. Representative immunoblots (left panels), and quantitative data (right panels) are shown. Data ( a , b ) are mean ± s.d. (n = 9 mice per group, 5 male, 4 female; age: 8 months). P-values were determined by the unpaired, two-tailed t-test (df=16; a , t = 9.4818, 4.9131; p = 5.7293e-08, p = 0.000156; b , t = 11.09, 0.3828; p = 6.42141e-09, p = 0.7069). c , Transcript levels of Ryr2 (left panel) and Atp2a2 (right panel) were determined by NGS in heart specimens of Tg- BBLN mice (Tg-1) and non-transgenic FVB mice. Data are mean ± s.d. (n = 4 male mice per group; age: 8 months). P-values were determined by the unpaired, two-tailed t-test (df=6; t = 7.4612, p = 0.000299 ( Ryr2 ); t = 33.28, p = 4.8989e-08 ( Atp2a2 )). d , BBLN transcript levels in right ventricular heart specimens of TOF patients with cyanosis were determined by microarray analysis (Affymetrix probe set ID: 204480_s_at) and negatively correlated with RYR2 (214044_at) and ATP2A2 (212361_s_at). Linear regression analysis was performed, and the Pearson correlation coefficient (r) and p-values (left panel, two-tailed, p = 0.0412; right panel, one-tailed, p = 0.0486) were determined (n = 11 TOF patients with cyanosis, 7 females, 4 males; age: 23.2 ± 5 months).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Western Blot, Transgenic Assay, Control, Two Tailed Test, Microarray, One-tailed Test
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Autophosphorylation of CAMK2D on T287 in the absence (Cont.) and presence of BBLN, BBLN-Mut1, BBLN-Mut2, and BBLN-SxxA (P-values vs. +BBLN). b , Sequence alignment of BBLN (residues 55–74) with the prototypical CAMK2 kinase domain-interacting region of GRIN2B (residues 1295–1310), and the regulatory domain residues 275–294 of CAMK2D was performed with CLUSTAL O. Potential interaction sites with CAMK2(D) kinase domain (based on ref. ) are shown below the sequence alignment. c , Interaction of BBLN with CAMK2D kinase domain residues 8–275 is strongly reduced in the presence of the GRIN2B peptide (30 μM). CAMK2D kinase domain was immobilized on anti-FLAG affinity matrix (AP) and incubated with BBLN in the absence and presence of GRIN2B peptide or control peptide. After washing steps and protein elution with SDS-PAGE sample buffer, BBLN was detected by immunoblot (IB) with anti-BBLN antibody, and CAMK2D was detected by anti-CAMK2D antibody (lower blot) (P-value vs. no peptide and +Cont. pept.). d , In vitro phosphorylation assay of BBLN, BBLN-SxxA, BBLN-Mut1 and BBLN-Mut2 by CAMK2D. Phospho-site-deficient BBLN-SxxA was not phosphorylated (BBLN wild-type set to 100 %). e , Interaction of BBLN, BBLN-SxxA, BBLN-Mut1, and BBLN-Mut2 with CAMK2D residues 8–275 was determined by binding assay. CAMK2D kinase domain was immobilized on anti-Flag affinity matrix (AP), and incubated with BBLN and different BBLN mutants. After washing steps, proteins were eluted and quantitated by immunoblot (IB) (P-value vs. BBLN, BBLN-Mut1 and BBLN-Mut2). Data are mean ± s.d ( a , d , n = 3; c , e , n = 4). P-values were determined by one-way ANOVA and Tukey’s test ( a , F(4,10) = 69.97; p = 0.03874, 0.05538, 0.000003179, 6.453e-7 vs.+BBLN; c , F(2,9) = 40.32; p = 0.00003353 and 0.0002668 + GRIN2B pept. vs. no peptide and +Cont. pept. d , F(3,8) = 64.42; p = 0.000003474, 0.00164, 0.001832 vs. BBLN; e , F(3,12) = 34.40; p = 0.000003081, 0.00002688, and 0.000255 SxxA vs. BBLN, Mut1, and Mut2).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Sequencing, Incubation, Control, SDS Page, Western Blot, In Vitro, Phosphorylation Assay, Binding Assay
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Cardiac contents of BBLN, phospho-T287-CAMK2D, and total CAMK2D were determined by immunoblot (IB) of cardiac proteins in heart specimen lysates from cyanotic and acyanotic TOF patients. The left panels show immunoblot images, and the right panels show quantitative data. The lower control immunoblot detects ATP5A1. b , Immunoblot detection of MLKL and phospho-S358-MLKL octamers in heart specimen lysates of cyanotic and acyanotic TOF patients. Data ( a , b ) are mean ± s.d. P-values were determined by the unpaired, two-tailed t-test (n = 6 patients per group, 3 females, 3 males; age cyanotic TOF patients: 23.17 ± 4.5 months; age acyanotic TOF patients: 29.5 ± 7.6 months; df=10; a , t = 6.0614, 4.4782, 0.6390; p = 0.0001218, 0.001182, 0.5372; b , t = 8.4943, 7.09; p = 0.000006939, 0.00003335). c , Correlation analyses were performed between cardiac contents of BBLN and total CAMK2D (left), BBLN and phospho-T287-CAMK2D (middle), and BBLN and phospho-S358-MLKL (right). Pearson correlation (r) and p-values (two-tailed) were determined of n = 6 cyanotic and 6 acyanotic TOF patients (left panel: p = 0.9209; middle panel: p = 0.0007209; right panel: p = 1.095e-7).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Western Blot, Control, Two Tailed Test
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Upregulated cardiac inflammasome transcripts in transgenic, 8-month-old, male Tg- BBLN mice (Tg-1) compared with age- and sex-matched, nontransgenic FVB mice were identified by Gene Ontology (GO) analysis of NGS transcriptome data. The heat map shows members of the canonical inflammasome complex (GO: 0061702) and proinflammatory CAMK2D-regulated transcripts of ref. . P values were determined by MeV (unpaired, two-tailed t -test, just alpha; n = 4 mice per group; d.f. 6; P = 0.005223, 0.003382, 0.001927, 0.000451, 8.083 × 10 −7 , 0.00000128, 0.01809, 0.00009222, 0.002207, 4.136 × 10 −7 , 0.000005349 and 4.188 × 10 −7 ). b , NGS data of prototypical transcripts involved in fibrotic cardiac remodeling of 8-month-old, male Tg- BBLN mice (Tg-1) compared with age- and sex-matched nontransgenic FVB mice. P values were determined by an unpaired, two-tailed t -test ( n = 4 mice per group; d.f. 6; t = 70.86, 47.35, 40.73 and 0.7437; P = 5.316 × 10 −10 , 5.946 × 10 −9 , 1.465 × 10 −8 and 0.4851). c , Picrosirius red staining of paraffin-embedded heart sections shows prominent fibrotic cardiac remodeling of 8-month-old, male Tg- BBLN mice (Tg-1) compared with age- and sex-matched, nontransgenic FVB mice ( n = 4 mouse hearts per group; scale bar, 2 mm).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Transgenic Assay, Two Tailed Test, Staining
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Cardiac contents of DES were determined by IB analysis of cardiac lysates prepared from male, 8-month-old Tg- BBLN (Tg-2) and Tg- BBLN –SxxA mice. b , IB detection of cardiac DES was performed in male, 8-month-old Tg- BBLN mice (Tg-2) without and with lentiviral transduction of an miRNA targeting Camk2d by RNAi (+miCamk2d). IB images (left) and quantitative IB data (right) of intact DES and the major DES fragment. Control IBs detect ATP5A1. Data are mean ± s.d. ( n = 6 mice per group). P values were determined by an unpaired, two-tailed t -test (d.f. 10; a , t = 4.870 and 5.281; P = 0.0006519 and 0.0003571; b , t = 5.825 and 10.40; P = 0.0001673 and 0.000001111).
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Transduction, Control, Two Tailed Test
Journal: Nature Cardiovascular Research
Article Title: BBLN triggers CAMK2D pathology in mice under cardiac pressure overload and potentially in unrepaired hearts with tetralogy of Fallot
doi: 10.1038/s44161-023-00351-6
Figure Lengend Snippet: a , Quantitative IB determination of cardiac contents of BBLN and activated phospho-T287–CAMK2D and total CAMK2D in male, 4-month-old B6 mice with 2 months of AAC, 4-month-old B6-miBbln mice with 2 months of AAC (AAC+miBbln) and 4-month-old sham-operated B6 mice (sham). IB images (left) and quantitative IB data (right). The lower control blot detects ATP5A1. b , IB determination of cardiac phospho-S345–MLKL (upper) and total MLKL (lower) contents of male, 4-month-old B6 mice with 2 months of AAC (AAC), 4-month-old B6-miBbln mice with 2 months of AAC (AAC+miBbln) and 4-month-old sham-operated B6 mice (sham). Predominant MLKL octamers as a feature of necroptosis were quantified. MLKL octamers (O), tetramers (T) and monomers (M) are marked with arrows. IB images (left) and quantitative IB data (right). c , Immunofluorescence colocalization of BBLN with p-S345–MLKL on heart specimens of a 4-month-old B6 mouse with 2 months of AAC (AAC), a 4-month-old B6-miBbln mouse with 2 months of AAC (AAC+miBbln) and a 4-month-old sham-operated B6 mouse (sham). The immunofluorescence is representative of four mouse hearts per group (scale bar, 40 μm). d , The left ventricular EF and the LVIDd were determined by echocardiography. Data are mean ± s.d. ( n = 6 male mice per group; one-way ANOVA and Tukey’s test; a , F (2,15) = 379.4, 354.4 and 32.97; top: P = 0, 1.246 × 10 −12 and 0.09708; middle: P = 1.727 × 10 −12 , 3.11 × 10 −13 and 0.3463; bottom: P = 0.003928, 0.000002048 and 0.001971; b , F (2,15) = 458.4 and 31.79; top: P = 0, 0 and 0.808; bottom: P = 0.00002672, 0.00000835 and 0.7711. d , F (2,15) = 28.47 and 15.68; top: P = 0.0005565, 0.000006051 and 0.05481; bottom: P = 0.0009046, 0.000402 and 0.9084.
Article Snippet: The following antibodies were used for IB detection, immunohistochemistry and immunofluorescence: rabbit monoclonal anti-ATP2A2/SERCA2 antibody (9580; D51B11; Cell Signaling Technology); rabbit polyclonal anti-C9orf16 (anti-BBLN) antibodies (HPA020725; Prestige Antibodies; Sigma Life Sciences);
Techniques: Control, Immunofluorescence
Journal: Journal of Investigative Medicine
Article Title: MiR-3150b inhibits hepatocellular carcinoma cell proliferation, migration and invasion by targeting GOLPH3
doi: 10.1136/jim-2019-001181
Figure Lengend Snippet: Expression of miR-3150b was downregulated in HCC cell lines. Relative mRNA expression of miR-3150b normal liver HL7702 cells and four GC cell lines with different differentiation status (MHCC-97L, HepG2, SMMC-7721 and SNU-398) determined by quantitative RT-PCR. All experiments were performed in triplicate with at least three independent experiments. Data were presented as the mean±SD. * p<0.05, ** p<0.01 vs HL7702 cells. GOLPH3, Golgi phosphoprotein 3; HCC, hepatocellular carcinoma.
Article Snippet: The blots were incubated with
Techniques: Expressing, Quantitative RT-PCR
Journal: Journal of Investigative Medicine
Article Title: MiR-3150b inhibits hepatocellular carcinoma cell proliferation, migration and invasion by targeting GOLPH3
doi: 10.1136/jim-2019-001181
Figure Lengend Snippet: MiR-3150b suppressed HCC cell proliferation relative miR-3150b expression (A) and CCK-8 cell viability assay (B) in HepG2 cells with transfection of miR-3150b mimic or si-GOLPH3, and in SNU-398 cells transfected with miR-3150b inhibitor or pcDNA3.1-GOLPH3. All experiments were performed in triplicate with at least three independent experiments. Data were presented as the mean±SD. ** p<0.01 vs mimic NC or inhibitor NC group. CCK-8, Cell Counting Kit-8; GOLPH3, Golgi phosphoprotein 3; HCC, hepatocellular carcinoma; NC, negative control.
Article Snippet: The blots were incubated with
Techniques: Expressing, CCK-8 Assay, Viability Assay, Transfection, Cell Counting, Negative Control
Journal: Journal of Investigative Medicine
Article Title: MiR-3150b inhibits hepatocellular carcinoma cell proliferation, migration and invasion by targeting GOLPH3
doi: 10.1136/jim-2019-001181
Figure Lengend Snippet: GOLPH3 was a direct target of miR-3150b. (A) alignment of miR-3150b with GOLPH3 3'-UTR sequences. HEK293T cells were co-transfected with luciferase reporter with wild-type (WT) GOLPH3 3'-UTR or with mutant GOLPH3 3'-UTR, and miR-3150b or mimic NC for 48 hours. The relative luciferase activity was analyzed by luciferase assay. The mRNA (B) and protein (C) levels of GOLPH3 in HepG2 cells transfected with miR-3150b mimic or mimic NC, and SNU-398 cells transfected with miR-3150b inhibitor or inhibitor NC using quantitative RT-PCR and western blot analysis. All experiments were performed in triplicate with at least three independent experiments. Data were presented as the mean±SD. ** p<0.01, *** p<0.001 vs mimic NC or inhibitor NC group. GOLPH3, Golgi phosphoprotein 3; HCC, hepatocellular carcinoma; NC, negative control; UTR, untranslated region.
Article Snippet: The blots were incubated with
Techniques: Transfection, Luciferase, Mutagenesis, Activity Assay, Quantitative RT-PCR, Western Blot, Negative Control
Journal: International Orthopaedics
Article Title: Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin–Beck disease and primary osteoarthritis
doi: 10.1007/s00264-013-1937-y
Figure Lengend Snippet: Chondrocyte gene network of CSGalNAcT-1 was classified as glycan biosynthesis and metabolism and functional pathway
Article Snippet: For the primary antibody,
Techniques: Functional Assay
Journal: International Orthopaedics
Article Title: Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin–Beck disease and primary osteoarthritis
doi: 10.1007/s00264-013-1937-y
Figure Lengend Snippet: CSGalNAcT-1 and Hapln-1 mRNA expression in osteoarthritis (OA) cartilage, Kashin-Beck disease (KBD) cartilage and normal cartilage. CSGalNAcT-1 and Hapln-1 mRNA levels reach statistical significance. * Denotes significant difference at P < 0.05
Article Snippet: For the primary antibody,
Techniques: Expressing
Journal: International Orthopaedics
Article Title: Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin–Beck disease and primary osteoarthritis
doi: 10.1007/s00264-013-1937-y
Figure Lengend Snippet: Comparison of CSGalNAcT-1 expression in the cartilage from osteoarthritis (OA), Kashin-Beck disease (KBD) and normal groups. a , b , c Denote the upper of normal, OA and KBD cartilage, respectively. d , e , f Denote the middle of normal, OA and KBD cartilage, respectively. g , h , i Denote the deep of normal, OA and KBD cartilage, respectively
Article Snippet: For the primary antibody,
Techniques: Expressing
Journal: International Orthopaedics
Article Title: Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and Hapln-1 in cartilage with Kashin–Beck disease and primary osteoarthritis
doi: 10.1007/s00264-013-1937-y
Figure Lengend Snippet: CSGalNAcT-1 and Hapln-1 protein level expression reduced in osteoarthritis (OA) and Kashin-Beck disease (KBD) cartilage compared with normal controls. Wnt 3a, β-catenin and Runx-2 level expression increased in OA and KBD cartilage compared with normal controls. A KBD free-Se group. B 0.25 μg/ml Se + KBD group. C 0.10 μg/ml Se + KBD group. D 0.05 μg/ml Se + KBD group
Article Snippet: For the primary antibody,
Techniques: Expressing