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TaKaRa template complementary dna cdna
Template Complementary Dna Cdna, supplied by TaKaRa, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 88 stars, based on 1 article reviews
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template complementary dna cdna - by Bioz Stars, 2020-09
88/100 stars

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SYBR Green Assay:

Article Title: Ecklonia Cava Extract Attenuates Endothelial Cell Dysfunction by Modulation of Inflammation and Brown Adipocyte Function in Perivascular Fat Tissue
Article Snippet: .. Appropriate primers (listed in ), distilled water and the RNA sample were mixed and placed in a 384-well plate followed by the addition of additional template complementary DNA (cDNA) and SYBR green (TAKARA, Japan). .. Mixed samples were validated using a PCR machine (Bio-Rad, CA, USA)

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Article Title: Circular RNAs expression profiles in plasma exosomes from early-stage lung adenocarcinoma and the potential biomarkers.
Article Snippet: .. This study aimed to identify differential circular RNA (circRNA) in the plasma exosomes of patients with lung adenocarcinoma (LUAD) using high-throughput sequencing. .. This study aimed to identify differential circular RNA (circRNA) in the plasma exosomes of patients with lung adenocarcinoma (LUAD) using high-throughput sequencing.

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  • 85
    TaKaRa tissue cdna templates
    <t>RNA</t> isolation, <t>cDNA</t> synthesis, and real-time PCR quantification
    Tissue Cdna Templates, supplied by TaKaRa, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tissue cdna templates/product/TaKaRa
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    85
    TaKaRa mutant mouse decorin cdna
    952delT Dcn transgenic mice express both wild-type and mutant <t>decorin.</t> A: Two independent families with human CSCD have been reported. A single base pair deletion in the coding sequence at either 941 (delC) or 967 (delT) caused frameshift mutations and a truncation of the C-terminal 33 amino acids. In mice, a delG at 926 or a delT at 952 (highlighted in red) will result in a comparable frameshift mutation. The new stop codon TGA (highlighted in red) will yield a C-terminal truncated decorin comparable to that in human CSCD. B: A Cre-on approach was used to create a transgenic mouse carrying a mutant decorin <t>cDNA</t> with a deleted T at 952. A stop codon flanked with LoxP ( red triangle ) elements was inserted between a ubiquitous CAG promoter and the mutant decorin cDNA. Corneal stromal targeting of mutant decorin was generated through breeding with Kera -cre mouse. The mouse model was bred into different backgrounds, including decorin wild-type, heterozygous, and deficient backgrounds. C: Immunoblot analyses show that the transgenic mice in a decorin wild-type background expresses two decorin bands after sequential Chondroitinase ABC and PNGase F digestion, one migrating with the wild-type decorin core, the other migrating faster at ∼37 kDa, consistent with the C-terminal truncation. The level of mutant decorin was substantially less than the wild-type decorin. These qualitative immunoblots were overloaded/exposed to show the presence or absence of the truncated decorin core in mutant and wild-type corneas, respectively. The antibody used was generated against the N-terminal 17 amino acids of the decorin protein core and thus recognizes both the native and the C-terminal–truncated species. D: Breeding the mutant into a decorin-null background allowed the localization of the mutant protein core. Mutant decorin expression was identified by immunolocalization in a 952delT Dcn mouse in decorin-deficient background ( yellow arrow indicates the positive reactivity of mutant decorin in the corneal stroma). Scale bar = 25 μm.
    Mutant Mouse Decorin Cdna, supplied by TaKaRa, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    TaKaRa cdna synthesis
    Testing the BPIV3 LFD RT-RPA assay for analytical specificity. (A) Specificity of the LFD RT-RPA assay. RPA products detected using LFD assay yield visually positive results only when tested using <t>cDNA</t> synthesis from BPIV3; results are visually negative for all other bovine viral pathogens with similar clinical symptoms. Samples were tested in triplicate with one reaction displayed in figure for each triplicate. (B) The results of amplification products of the LFD RT-RPA on 2% agarose gel. Lanes 1 to 6: BEFV, VSV, BcoV, BRSV, BVDV, and IBRV, respectively; Lane 7: positive control of BPIV3. (C) Quality detection of <t>RNA/DNA</t> of BEFV, VSV, BcoV, BRSV, BVDV, IBRV and BPIV3. The RNA/DNA of different virus was prepared for specificity detection by PCR reaction with viral specific primers. The positive amplification results were shown in Lane 2, Lane 4, Lane 6, Lane 8, Lane 10, Lane 12, Lane 14, respectively. Lane 1, Lane 3, Lane 5, Lane 7, Lane 9, Lane 11, Lane 13 were negative controls with DNase-free water as template.
    Cdna Synthesis, supplied by TaKaRa, used in various techniques. Bioz Stars score: 94/100, based on 312 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    TaKaRa mouse brain cdna template
    Tissue distribution of the mouse and monkey UT receptor: (a) Tissue distribution of mouse UT receptor <t>cDNA</t> transcripts by RT – <t>PCR</t> revealed expression within cardiac and vascular (thoracic but not abdominal aorta) tissue in addition to bladder and pancreas. Trace levels of expression are also observed in skeletal muscle, oesophagus, lung and adipose tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (Lower panel) by Southern analysis using full-length UT receptor cDNA probe. (b) Tissue distributions of monkey UT receptor cDNA transcripts by RT – PCR revealed expression within heart (ventricle > atrium) and arterial blood vessels (aorta not vena cava), pancreas. Detectable levels of expression were also observed in the skeletal muscle, lung, thyroid and adrenal glands, kidney, upper portions of the gastrointestinal tract (oesophagus, stomach and small intestine but not colonic tissue) and spinal cord (but not in the cortical or cerebellar samples isolated). No detectable transcripts were derived from hepatic, bladder, adipose tissue or splenic tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (lower panel) by Southern analysis using full-length UT receptor cDNA probe.
    Mouse Brain Cdna Template, supplied by TaKaRa, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse brain cdna template/product/TaKaRa
    Average 98 stars, based on 1 article reviews
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    RNA isolation, cDNA synthesis, and real-time PCR quantification

    Journal:

    Article Title: Species differences in cannabinoid receptor 2 (CNR2 gene): identification of novel human and rodent CB2 isoforms, differential tissue expression, and regulation by cannabinoid receptor ligands

    doi: 10.1111/j.1601-183X.2009.00498.x

    Figure Lengend Snippet: RNA isolation, cDNA synthesis, and real-time PCR quantification

    Article Snippet: The tissue cDNA templates were synthesized from human RNA preparations that consist of intact RNA with no genomic DNA contamination (Clontech, Mountain View, CA).

    Techniques: Isolation, Real-time Polymerase Chain Reaction

    952delT Dcn transgenic mice express both wild-type and mutant decorin. A: Two independent families with human CSCD have been reported. A single base pair deletion in the coding sequence at either 941 (delC) or 967 (delT) caused frameshift mutations and a truncation of the C-terminal 33 amino acids. In mice, a delG at 926 or a delT at 952 (highlighted in red) will result in a comparable frameshift mutation. The new stop codon TGA (highlighted in red) will yield a C-terminal truncated decorin comparable to that in human CSCD. B: A Cre-on approach was used to create a transgenic mouse carrying a mutant decorin cDNA with a deleted T at 952. A stop codon flanked with LoxP ( red triangle ) elements was inserted between a ubiquitous CAG promoter and the mutant decorin cDNA. Corneal stromal targeting of mutant decorin was generated through breeding with Kera -cre mouse. The mouse model was bred into different backgrounds, including decorin wild-type, heterozygous, and deficient backgrounds. C: Immunoblot analyses show that the transgenic mice in a decorin wild-type background expresses two decorin bands after sequential Chondroitinase ABC and PNGase F digestion, one migrating with the wild-type decorin core, the other migrating faster at ∼37 kDa, consistent with the C-terminal truncation. The level of mutant decorin was substantially less than the wild-type decorin. These qualitative immunoblots were overloaded/exposed to show the presence or absence of the truncated decorin core in mutant and wild-type corneas, respectively. The antibody used was generated against the N-terminal 17 amino acids of the decorin protein core and thus recognizes both the native and the C-terminal–truncated species. D: Breeding the mutant into a decorin-null background allowed the localization of the mutant protein core. Mutant decorin expression was identified by immunolocalization in a 952delT Dcn mouse in decorin-deficient background ( yellow arrow indicates the positive reactivity of mutant decorin in the corneal stroma). Scale bar = 25 μm.

    Journal: The American Journal of Pathology

    Article Title: Pathophysiological Mechanisms of Autosomal Dominant Congenital Stromal Corneal Dystrophy

    doi: 10.1016/j.ajpath.2011.07.026

    Figure Lengend Snippet: 952delT Dcn transgenic mice express both wild-type and mutant decorin. A: Two independent families with human CSCD have been reported. A single base pair deletion in the coding sequence at either 941 (delC) or 967 (delT) caused frameshift mutations and a truncation of the C-terminal 33 amino acids. In mice, a delG at 926 or a delT at 952 (highlighted in red) will result in a comparable frameshift mutation. The new stop codon TGA (highlighted in red) will yield a C-terminal truncated decorin comparable to that in human CSCD. B: A Cre-on approach was used to create a transgenic mouse carrying a mutant decorin cDNA with a deleted T at 952. A stop codon flanked with LoxP ( red triangle ) elements was inserted between a ubiquitous CAG promoter and the mutant decorin cDNA. Corneal stromal targeting of mutant decorin was generated through breeding with Kera -cre mouse. The mouse model was bred into different backgrounds, including decorin wild-type, heterozygous, and deficient backgrounds. C: Immunoblot analyses show that the transgenic mice in a decorin wild-type background expresses two decorin bands after sequential Chondroitinase ABC and PNGase F digestion, one migrating with the wild-type decorin core, the other migrating faster at ∼37 kDa, consistent with the C-terminal truncation. The level of mutant decorin was substantially less than the wild-type decorin. These qualitative immunoblots were overloaded/exposed to show the presence or absence of the truncated decorin core in mutant and wild-type corneas, respectively. The antibody used was generated against the N-terminal 17 amino acids of the decorin protein core and thus recognizes both the native and the C-terminal–truncated species. D: Breeding the mutant into a decorin-null background allowed the localization of the mutant protein core. Mutant decorin expression was identified by immunolocalization in a 952delT Dcn mouse in decorin-deficient background ( yellow arrow indicates the positive reactivity of mutant decorin in the corneal stroma). Scale bar = 25 μm.

    Article Snippet: A pMSCV/Dec plasmid, which contains pMSCVpuro (Clontech, Mountain View CA) vector, and a full-length mouse decorin cDNA, was used as the template for making the mutant mouse decorin cDNA (952 delT) with the use of a Transformer Site-directed mutagenesis kit (Clontech).

    Techniques: Transgenic Assay, Mouse Assay, Mutagenesis, Sequencing, Generated, Western Blot, Expressing

    Testing the BPIV3 LFD RT-RPA assay for analytical specificity. (A) Specificity of the LFD RT-RPA assay. RPA products detected using LFD assay yield visually positive results only when tested using cDNA synthesis from BPIV3; results are visually negative for all other bovine viral pathogens with similar clinical symptoms. Samples were tested in triplicate with one reaction displayed in figure for each triplicate. (B) The results of amplification products of the LFD RT-RPA on 2% agarose gel. Lanes 1 to 6: BEFV, VSV, BcoV, BRSV, BVDV, and IBRV, respectively; Lane 7: positive control of BPIV3. (C) Quality detection of RNA/DNA of BEFV, VSV, BcoV, BRSV, BVDV, IBRV and BPIV3. The RNA/DNA of different virus was prepared for specificity detection by PCR reaction with viral specific primers. The positive amplification results were shown in Lane 2, Lane 4, Lane 6, Lane 8, Lane 10, Lane 12, Lane 14, respectively. Lane 1, Lane 3, Lane 5, Lane 7, Lane 9, Lane 11, Lane 13 were negative controls with DNase-free water as template.

    Journal: Molecular and Cellular Probes

    Article Title: A lateral flow dipstick combined with reverse transcription recombinase polymerase amplification for rapid and visual detection of the bovine respirovirus 3

    doi: 10.1016/j.mcp.2018.08.004

    Figure Lengend Snippet: Testing the BPIV3 LFD RT-RPA assay for analytical specificity. (A) Specificity of the LFD RT-RPA assay. RPA products detected using LFD assay yield visually positive results only when tested using cDNA synthesis from BPIV3; results are visually negative for all other bovine viral pathogens with similar clinical symptoms. Samples were tested in triplicate with one reaction displayed in figure for each triplicate. (B) The results of amplification products of the LFD RT-RPA on 2% agarose gel. Lanes 1 to 6: BEFV, VSV, BcoV, BRSV, BVDV, and IBRV, respectively; Lane 7: positive control of BPIV3. (C) Quality detection of RNA/DNA of BEFV, VSV, BcoV, BRSV, BVDV, IBRV and BPIV3. The RNA/DNA of different virus was prepared for specificity detection by PCR reaction with viral specific primers. The positive amplification results were shown in Lane 2, Lane 4, Lane 6, Lane 8, Lane 10, Lane 12, Lane 14, respectively. Lane 1, Lane 3, Lane 5, Lane 7, Lane 9, Lane 11, Lane 13 were negative controls with DNase-free water as template.

    Article Snippet: The extracted RNA was used as template for cDNA synthesis using reverse transcription with random primers according to the instructions of the PrimeScript RT Master Mix (TaKaRa, Dalian, China).

    Techniques: RT RPA Assay, Recombinase Polymerase Amplification, Amplification, Agarose Gel Electrophoresis, Positive Control, Polymerase Chain Reaction

    Tissue distribution of the mouse and monkey UT receptor: (a) Tissue distribution of mouse UT receptor cDNA transcripts by RT – PCR revealed expression within cardiac and vascular (thoracic but not abdominal aorta) tissue in addition to bladder and pancreas. Trace levels of expression are also observed in skeletal muscle, oesophagus, lung and adipose tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (Lower panel) by Southern analysis using full-length UT receptor cDNA probe. (b) Tissue distributions of monkey UT receptor cDNA transcripts by RT – PCR revealed expression within heart (ventricle > atrium) and arterial blood vessels (aorta not vena cava), pancreas. Detectable levels of expression were also observed in the skeletal muscle, lung, thyroid and adrenal glands, kidney, upper portions of the gastrointestinal tract (oesophagus, stomach and small intestine but not colonic tissue) and spinal cord (but not in the cortical or cerebellar samples isolated). No detectable transcripts were derived from hepatic, bladder, adipose tissue or splenic tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (lower panel) by Southern analysis using full-length UT receptor cDNA probe.

    Journal: British Journal of Pharmacology

    Article Title: Molecular and pharmacological characterization of genes encoding urotensin-II peptides and their cognate G-protein-coupled receptors from the mouse and monkey

    doi: 10.1038/sj.bjp.0704671

    Figure Lengend Snippet: Tissue distribution of the mouse and monkey UT receptor: (a) Tissue distribution of mouse UT receptor cDNA transcripts by RT – PCR revealed expression within cardiac and vascular (thoracic but not abdominal aorta) tissue in addition to bladder and pancreas. Trace levels of expression are also observed in skeletal muscle, oesophagus, lung and adipose tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (Lower panel) by Southern analysis using full-length UT receptor cDNA probe. (b) Tissue distributions of monkey UT receptor cDNA transcripts by RT – PCR revealed expression within heart (ventricle > atrium) and arterial blood vessels (aorta not vena cava), pancreas. Detectable levels of expression were also observed in the skeletal muscle, lung, thyroid and adrenal glands, kidney, upper portions of the gastrointestinal tract (oesophagus, stomach and small intestine but not colonic tissue) and spinal cord (but not in the cortical or cerebellar samples isolated). No detectable transcripts were derived from hepatic, bladder, adipose tissue or splenic tissue. (Middle panel) Amplification of GAPDH cDNA did not differ significantly between tissues. The specificity of the RT – PCR amplification of UT receptor transcripts was confirmed (lower panel) by Southern analysis using full-length UT receptor cDNA probe.

    Article Snippet: These primers were used to obtain the full-length preproU-II complementary DNA (cDNA) clone from mouse brain cDNA template (Clonetech) by polymerase chain reaction (PCR).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Amplification, Isolation, Derivative Assay

    Tissue distribution of the mouse and monkey U-II. (a): Tissue distribution of mouse preproU-II cDNA transcripts by RT – PCR revealed expression within heart, thoracic aorta, testes, brain, skeletal muscle, liver, kidney and spleen (upper panel). Negligible expression of preproU-II was observed in the mouse gastrointestinal tract (stomach, oesophagus, small intestine and colon), bladder, pancreas, adrenal, lung and adipose tissue. Amplification of GAPDH cDNA did not differ significantly between tissues (middle panel). The specificity of the RT – PCR amplification of preproU-II transcripts was confirmed by Southern analysis using full-length preproU-II cDNA probe (lower panel). (b) Tissue distribution of monkey preproU-II cDNA transcripts by RT – PCR revealed expression within heart (ventricle and atrium), thoracic aorta, CNS (spinal cord, cerebellum and cortex), skeletal muscle, kidney, liver and spleen (upper panel). No detectable transcripts were derived from vena cava, endocrine tissues including thyroid, pancreas and adrenal glands, lung, gastrointestinal tissue (oesophagus, stomach, small intestine, colon), bladder or adipose tissue. Amplification of GAPDH cDNA did not differ significantly between tissues (middle panel). The specificity of the RT – PCR amplification of preproU-II transcripts was confirmed by Southern analysis using full-length preproU-II cDNA probe (lower panel).

    Journal: British Journal of Pharmacology

    Article Title: Molecular and pharmacological characterization of genes encoding urotensin-II peptides and their cognate G-protein-coupled receptors from the mouse and monkey

    doi: 10.1038/sj.bjp.0704671

    Figure Lengend Snippet: Tissue distribution of the mouse and monkey U-II. (a): Tissue distribution of mouse preproU-II cDNA transcripts by RT – PCR revealed expression within heart, thoracic aorta, testes, brain, skeletal muscle, liver, kidney and spleen (upper panel). Negligible expression of preproU-II was observed in the mouse gastrointestinal tract (stomach, oesophagus, small intestine and colon), bladder, pancreas, adrenal, lung and adipose tissue. Amplification of GAPDH cDNA did not differ significantly between tissues (middle panel). The specificity of the RT – PCR amplification of preproU-II transcripts was confirmed by Southern analysis using full-length preproU-II cDNA probe (lower panel). (b) Tissue distribution of monkey preproU-II cDNA transcripts by RT – PCR revealed expression within heart (ventricle and atrium), thoracic aorta, CNS (spinal cord, cerebellum and cortex), skeletal muscle, kidney, liver and spleen (upper panel). No detectable transcripts were derived from vena cava, endocrine tissues including thyroid, pancreas and adrenal glands, lung, gastrointestinal tissue (oesophagus, stomach, small intestine, colon), bladder or adipose tissue. Amplification of GAPDH cDNA did not differ significantly between tissues (middle panel). The specificity of the RT – PCR amplification of preproU-II transcripts was confirmed by Southern analysis using full-length preproU-II cDNA probe (lower panel).

    Article Snippet: These primers were used to obtain the full-length preproU-II complementary DNA (cDNA) clone from mouse brain cDNA template (Clonetech) by polymerase chain reaction (PCR).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Amplification, Derivative Assay