k atpase α 1 subunit Search Results


na,k-atpase α 1 subunit monoclonal antibody clone 464.6  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc na,k-atpase α 1 subunit monoclonal antibody clone 464.6
Na,K Atpase α 1 Subunit Monoclonal Antibody Clone 464.6, supplied by Upstate Biotechnology 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/result/na,k-atpase α 1 subunit monoclonal antibody clone 464.6/product/Upstate Biotechnology Inc
Average 90 stars, based on 1 article reviews
na,k-atpase α 1 subunit monoclonal antibody clone 464.6 - by Bioz Stars, 2026-03
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na+/k+ atpase α-1 subunit  (Merck KGaA)
90
Merck KGaA na+/k+ atpase α-1 subunit
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Na+/K+ Atpase α 1 Subunit, supplied by Merck KGaA, 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/result/na+/k+ atpase α-1 subunit/product/Merck KGaA
Average 90 stars, based on 1 article reviews
na+/k+ atpase α-1 subunit - by Bioz Stars, 2026-03
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mouse antina+–k+-atpase α1 subunit antibody  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc mouse antina+–k+-atpase α1 subunit antibody
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Mouse Antina+–K+ Atpase α1 Subunit Antibody, supplied by Upstate Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse antina+–k+-atpase α1 subunit antibody - by Bioz Stars, 2026-03
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anti-na+, k+-atpase-α1 subunit antibody  (Merck & Co)
90
Merck & Co anti-na+, k+-atpase-α1 subunit antibody
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Anti Na+, K+ Atpase α1 Subunit Antibody, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-na+, k+-atpase-α1 subunit antibody - by Bioz Stars, 2026-03
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na,k-atpase α1 and β-subunits  (Eppendorf AG)
90
Eppendorf AG na,k-atpase α1 and β-subunits
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Na,K Atpase α1 And β Subunits, supplied by Eppendorf AG, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
na,k-atpase α1 and β-subunits - by Bioz Stars, 2026-03
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anti-rat na + ,k + -atpase α1 subunit antibody  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc anti-rat na + ,k + -atpase α1 subunit antibody
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Anti Rat Na + ,K + Atpase α1 Subunit Antibody, supplied by Upstate Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-rat na + ,k + -atpase α1 subunit antibody raised against residues 338–518  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc anti-rat na + ,k + -atpase α1 subunit antibody raised against residues 338–518
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Anti Rat Na + ,K + Atpase α1 Subunit Antibody Raised Against Residues 338–518, supplied by Upstate Biotechnology 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/result/anti-rat na + ,k + -atpase α1 subunit antibody raised against residues 338–518/product/Upstate Biotechnology Inc
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anti-rat na + ,k + -atpase α1 subunit antibody raised against residues 338–518 - by Bioz Stars, 2026-03
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anti-na-k-atpase ( α 1-subunit)  (Merck KGaA)
90
Merck KGaA anti-na-k-atpase ( α 1-subunit)
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Anti Na K Atpase ( α 1 Subunit), supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-rat brain na, k-atpase α1 subunit antibody  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc anti-rat brain na, k-atpase α1 subunit antibody
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Anti Rat Brain Na, K Atpase α1 Subunit Antibody, supplied by Upstate Biotechnology 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/result/anti-rat brain na, k-atpase α1 subunit antibody/product/Upstate Biotechnology Inc
Average 90 stars, based on 1 article reviews
anti-rat brain na, k-atpase α1 subunit antibody - by Bioz Stars, 2026-03
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na+/k+ atpase α1 subunit  (Dawley Inc)
90
Dawley Inc na+/k+ atpase α1 subunit
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Na+/K+ Atpase α1 Subunit, supplied by Dawley Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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polyclonal antina+,k+-atpase α1 subunit  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc polyclonal antina+,k+-atpase α1 subunit
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Polyclonal Antina+,K+ Atpase α1 Subunit, supplied by Upstate Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sirna duplexes against human na+/k+-atpase α1 subunit  (Ribobio co)
90
Ribobio co sirna duplexes against human na+/k+-atpase α1 subunit
( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + <t>ATPase</t> α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.
Sirna Duplexes Against Human Na+/K+ Atpase α1 Subunit, supplied by Ribobio co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + ATPase α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.

Journal: PLoS ONE

Article Title: Sortilin-Related Receptor SORCS3 Is a Postsynaptic Modulator of Synaptic Depression and Fear Extinction

doi: 10.1371/journal.pone.0075006

Figure Lengend Snippet: ( A ) For targeted disruption of the murine Sorcs3 locus, a targeting vector was constructed introducing the neomycin phosphotransferase gene driven by the phosphoglycerate kinase promoter (PGK-neoR) into intron 2 of the Sorcs3 locus. The PGK-neoR cassette was flanked by FRT sites (open triangles). In addition, the vector introduced two loxP recombination sites (closed triangles) 5’ and 3’ of exon 1, respectively. Following standard homologous recombination in embryonic stem cells and blastocyst injections, mice carrying the modified gene through the germ line were bred with the flp deleter strain to remove PGK-neoR (targeted allele). For gene inactivation, mice were crossed with cre deleter mice to excise exon 1 that encodes the start codon and signal and pro-peptides of Sorcs3 (deleted allele). ( B ) RT-PCR analysis on brain tissue documents complete loss of transcripts encoding exon 1 in Sorcs3 -/- animals as compared to Sorcs3 +/+ controls. Minor amounts of an aberrant transcript encompassing exons 13-15 are seen. (C) Successful ablation of SORCS3 protein expression was confirmed by Western blot analysis of extracts from hippocampus (Hip), cortex (Ctx), and cerebellum (Cer) detecting SORCS3 in wild type mice (+/+), but in animals homozygous for the disrupted allele (-/-). Detection of Na + /K + ATPase α-1 subunit (Na/K) served as loading control. ( D ) Histological sections stained with Nissl from hippocampi of Sorcs3 +/+ and Sorcs3 -/- mice. ( E ) Western blot analysis of the indicated proteins in the PSD fraction of hippocampi from Sorcs3 +/+ and Sorcs3 -/- mice. NR 1/2 B, NMDA glutamate receptor subunit 1/2B; GluR1/2, AMPA glutamate receptor subunit 1/2; mGlur5, metabotropic glutamate receptor type 5; p75NTR, nerve growth factor receptor; TrkB, neurotrophic tyrosine kinase, receptor, type 2.

Article Snippet: Antisera directed against the following proteins were obtained from commercial suppliers: PDS95, GluR2, NR2B, mGluR5 (NeuroMab); synaptophysin (Synaptic Systems); GluR1, p75NTR, TrkB (Cell Signalling); PICK1 (Novus Biologicals, NeuroMab), Na + /K + ATPase α-1 subunit (Merck Millipore Cat. 05-369), SORCS2 (A. Nykjaer, Aarhus).

Techniques: Disruption, Plasmid Preparation, Construct, Homologous Recombination, Modification, Reverse Transcription Polymerase Chain Reaction, Expressing, Western Blot, Control, Staining