- PA5-29049 - Invitrogen Antibodies NPR1 antibody

Sun F, Zhou K, Tian KY, Zhang XY, Liu W, Wang J, Zhong CP, Qiu JH, Zha DJ
Frontiers in cell and developmental biology 2021;9:681421

Mezzasoma L, Talesa VN, Costanzi E, Bellezza I
Biomolecules 2021 May 25;11(6)

Sun F, Zhou K, Tian KY, Wang J, Qiu JH, Zha DJ
Neural plasticity 2020;2020:8831735

Mao YQ, Han SF, Zhang SL, Zhang ZY, Kong CY, Chen HL, Li ZM, Cai PR, Han B, Wang LS
Cell proliferation 2020 Jun;53(6):e12832

Mezzasoma L, Talesa VN, Romani R, Bellezza I
International journal of molecular sciences 2020 Dec 22;22(1)

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunofluorescent analysis of NPR-A in paraformaldehyde-fixed HeLa cells using a NPR-A polyclonal antibody (Product # PA5-29049) at a 1:200 dilution.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: 9 FIGURE NPR1, DCAF4L2 and TSSK6 expression is increased in glioma, and elevated NPR1 or TSSK6 expression is a prognostic indicator of poor survival in patients with classical glioma. A, NPR1, TSSK6 and DCAF4L2 mRNA expression in multiple tumour tissues and normal tissues based on RNA-Seq data from the TCGA. Log2-normalized read count (TPM) is shown. TPM, transcripts per kilobase of exon model per million mapped reads. B, mRNA expression of NPR1, DCAF4L2 and TSSK6 was analysed in glioma tissues from the TCGA data sets. C, Kaplan-Meier survival curve analysis indicated that patients with NPR1 and TSSK6 overexpression had a significantly shorter overall survival in the classical subtype of glioma. D, E, NPR1 protein expression levels were elevated in primary glioma patient samples. F, Immunohistochemical staining of NPR1 in glioma tissue

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 Immunolocalization of ANP, NPR-A, and NPR-C in SGNs within the SG of P14 rats. Merge and single-channel images of cochlear sections triple labeled with antibodies against neural marker TUJ1 (green), ANP/NPR-A/NPR-C (red), and DAPI (blue). (a) ANP was predominantly immunoreactive in the perikarya of SGNs. NPR-A (b) and NPR-C (c) were predominantly immunoreactive in the plasma membrane and cytoplasm of SGNs and appeared more pronounced in the cellular membrane. Scale bars = 50 mu m.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 Immunolocalization of ANP, NPR-A, and NPR-C in dissociated SGNs from P3 rats. Merge and single-channel images of SG cells triple labeled with antibodies against TUJ1 (green), ANP/NPR-A/NPR-C (red), and DAPI (blue). The immunoreactivity of ANP (a), NPR-A (b), or NPR-C (c) was colocalized with beta -III tubulin-positive SGNs, respectively, distributed in the neuronal soma and neurites. Scale bars = 50 mu m.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 Cyclic Guanossine monophosphate (cGMP)/Protein kinase G--I (PKG-I) axis drives Atrial natriuretic peptide (ANP)/ B-type natriuretic peptide (BNP) inhibitory effect on Interleukin (IL)-1beta secretion. THP-1 cells were treated with ANP or BNP (10 -8 M) ( A , B ) or 8-Br-cGMP (100 µM) ( C ) for 1 h ( A , C ) or 30 min ( B ). ( A , C ) NPR-1 protein expression by Western blot. Protein loading was assessed by re-probing the blots with an anti-beta-actin antibody. Western blots are representative of n = 3 independent experiments. ( B ) Cells were lysed, and cGMP intracellular levels were measured by ELISA assay (basal cGMP: 64 fmol/10 6 cells). ( D ) THP-1 cells, either pretreated for 10 min with ANP or BNP (10 -8 M) or 8-Br-cGMP (100 µM) or left untreated, were exposed to LPS (10 µg/mL) for 20 min and treated with ATP (5 mM) for 48 h. When used, KT-5823 (1muM) was added 1 h before ANP, BNP, or cGMP. The supernatants were collected and IL-1beta release was measured by ELISA. All histograms indicate mean +- SD of at least n = three independent experiments, each one tested in triplicate. * p < 0.05, ** p < 0.01, *** p < 0.001 versus untreated control cells; deg p < 0.05, degdeg p < 0.01, versus LPS + ATP-treated cells; # p < 0.05 versus KT-5823 + LPS + ATP treated cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4 ANP and BNP counteract PC3-derived EVs-induced inflammasome activation in PNT2 cells. Non-cancerous PNT2 cells were grown for 24 h. Cell lysates were immunoblotted for pro- IL-1beta and mature caspase-1-p20 ( A ); NPR-1, ANP, and BNP ( B ). PNT2 cells were pre-incubated with ANP or BNP (1 uM) for 10 min and then treated with PC3-derived EVs (PC3-EVs) (100 ug/mL) for a 24 h. Cell lysate were immunoblotted for NLRP3 ( C , D ), phospho-NLRP3 (Ser295) ( C , H ), caspase-1 ( C , E ), IL-1beta ( C , F , G ), phospho-ERK 1/2 or ERK 1/2 ( I ) and phospho-p38-MAPK or p38-MAPK ( J ). beta-actin or alpha-tubulin were used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. All histograms indicate the mean +- SD of at least n = 3 independent experiments, each one tested in triplicate. ** p < 0.01, *** p < 0.001 vs. untreated PC3 cells. # p < 0.05, ### p < 0.001 vs. PC3-EVs treated PC3 cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: FIGURE 2 Immunolocalization of ANP, NPR-A and NPR-C in SGNs within cochlear SG from rats at P7. (A-C) Gross view of cryosectioned cochlear tissues triple-labeled with antibodies against neural marker beta-III Tubulin (TUJ1, green), ANP/NPR-A/NPR-C (red) and Hoechst (blue). (A 1 ,B 1 ,C 1 ) High-magnification views of the boxed region of (A-C) . (A 2 ,B 2 ,C 2 ) Higher-magnification images of the boxed region of (A 1 ,B 1 ,C 1 ) reveal that ANP/NPR-A/NPR-C is colocalized with TUJ1-positive SGNs, respectively. (A 2' ,B 2' ,C 2' ) Immunoreactivities of ANP, NPR-A, and NPR-C are present in the SGNs. Scale bars = 100 mum.

PA5-29049