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rabbit anti human tert polyclonal antibody  (OriGene)


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    Structured Review

    OriGene rabbit anti human tert polyclonal antibody
    Rabbit Anti Human Tert Polyclonal Antibody, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti human tert polyclonal antibody/product/OriGene
    Average 94 stars, based on 2 article reviews
    rabbit anti human tert polyclonal antibody - by Bioz Stars, 2026-02
    94/100 stars

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    The odds ratios of  TERT  SNPs rs61748181 among rapid versus non-decliners in the LHS.

    Journal: Scientific Reports

    Article Title: Mild catalytic defects of tert rs61748181 polymorphism affect the clinical presentation of chronic obstructive pulmonary disease

    doi: 10.1038/s41598-021-83686-z

    Figure Lengend Snippet: The odds ratios of TERT SNPs rs61748181 among rapid versus non-decliners in the LHS.

    Article Snippet: A sheep anti-human TERT polyclonal antibody (0.5 μg/ml, Abbexa, Cambridge, UK) and a Donkey anti-sheep horseradish peroxidase-conjugated antibody (0.2 μg/ml, Jackson ImmunoResearch, West Grove, PA, USA) were sequentially applied before detection by ECL (PerkinElmer, Waltham, MA, USA) on Kodak X-ray films.

    Techniques:

    Restoration of recombinant telomerase mediated by the TERT variants in BJ cell lines. ( A ) Recombinant expression of TERT in BJ fibroblasts. TERT expression levels (127 kDa) were normalized to those of vinculin (124 kDa) and the data are presented as mean ± SEM (n = 6). fluorescent & ECL ones). TERT and vinculin signals were differentiated with the use of differently labeled antibodies (chemiluminescent and fluorescent, respectively) and processed accordingly with different detection modalities. Full sets of data were available in the supplementary information (Supplementary Fig. ) ( B ) Cellular growth kinetics of BJ cell lines expressing recombinant SNP-version of telomerase. ( C ) Telomere lengths in the cells at approximately every 10 PDLs were measured by TRF. Population doubling level (PDL) and telomere lengths (telomere restriction fragments, TRF) for each sample are illustrated. ( D ) Changes in telomere length over cell divisions are plotted.

    Journal: Scientific Reports

    Article Title: Mild catalytic defects of tert rs61748181 polymorphism affect the clinical presentation of chronic obstructive pulmonary disease

    doi: 10.1038/s41598-021-83686-z

    Figure Lengend Snippet: Restoration of recombinant telomerase mediated by the TERT variants in BJ cell lines. ( A ) Recombinant expression of TERT in BJ fibroblasts. TERT expression levels (127 kDa) were normalized to those of vinculin (124 kDa) and the data are presented as mean ± SEM (n = 6). fluorescent & ECL ones). TERT and vinculin signals were differentiated with the use of differently labeled antibodies (chemiluminescent and fluorescent, respectively) and processed accordingly with different detection modalities. Full sets of data were available in the supplementary information (Supplementary Fig. ) ( B ) Cellular growth kinetics of BJ cell lines expressing recombinant SNP-version of telomerase. ( C ) Telomere lengths in the cells at approximately every 10 PDLs were measured by TRF. Population doubling level (PDL) and telomere lengths (telomere restriction fragments, TRF) for each sample are illustrated. ( D ) Changes in telomere length over cell divisions are plotted.

    Article Snippet: A sheep anti-human TERT polyclonal antibody (0.5 μg/ml, Abbexa, Cambridge, UK) and a Donkey anti-sheep horseradish peroxidase-conjugated antibody (0.2 μg/ml, Jackson ImmunoResearch, West Grove, PA, USA) were sequentially applied before detection by ECL (PerkinElmer, Waltham, MA, USA) on Kodak X-ray films.

    Techniques: Recombinant, Expressing, Labeling

    The impact of genetic defects in telomere maintenance on lung function deterioration. Telomere Biology Diseases (TBD, right panel) are caused by rare genetic mutations that severely compromise the synthesis and/or the structural protection of the telomeres. TBD patients display extremely short telomeres at a young age, precipitating the onset of clinical symptoms. In contrast, carriers of common TERT genetic variants (SNPs) (middle panel) are not expected to display pathogenesis associated with short telomeres in the absence of additional factors (environmental, pathological or in combination with other genetic determinants) that accelerate telomere attritions. Even so, these carriers are still genetically predetermined to a decreased capacity to maintain their telomeres, when compared with noncarriers (left panel). These deficiencies, while silent phenotypically within the general population, could be unmasked by the massive increase in regenerative demand associated with tissue degenerative conditions, as seen in the case of COPD. Our work provides a proof-of-principle for novel epidemiological and clinical evaluations of the common SNPs in telomere biology genes on their effects as genetic modifiers rather than drivers of chronic tissue-degenerative disorders.

    Journal: Scientific Reports

    Article Title: Mild catalytic defects of tert rs61748181 polymorphism affect the clinical presentation of chronic obstructive pulmonary disease

    doi: 10.1038/s41598-021-83686-z

    Figure Lengend Snippet: The impact of genetic defects in telomere maintenance on lung function deterioration. Telomere Biology Diseases (TBD, right panel) are caused by rare genetic mutations that severely compromise the synthesis and/or the structural protection of the telomeres. TBD patients display extremely short telomeres at a young age, precipitating the onset of clinical symptoms. In contrast, carriers of common TERT genetic variants (SNPs) (middle panel) are not expected to display pathogenesis associated with short telomeres in the absence of additional factors (environmental, pathological or in combination with other genetic determinants) that accelerate telomere attritions. Even so, these carriers are still genetically predetermined to a decreased capacity to maintain their telomeres, when compared with noncarriers (left panel). These deficiencies, while silent phenotypically within the general population, could be unmasked by the massive increase in regenerative demand associated with tissue degenerative conditions, as seen in the case of COPD. Our work provides a proof-of-principle for novel epidemiological and clinical evaluations of the common SNPs in telomere biology genes on their effects as genetic modifiers rather than drivers of chronic tissue-degenerative disorders.

    Article Snippet: A sheep anti-human TERT polyclonal antibody (0.5 μg/ml, Abbexa, Cambridge, UK) and a Donkey anti-sheep horseradish peroxidase-conjugated antibody (0.2 μg/ml, Jackson ImmunoResearch, West Grove, PA, USA) were sequentially applied before detection by ECL (PerkinElmer, Waltham, MA, USA) on Kodak X-ray films.

    Techniques: