l paracasei atcc 25598 Search Results


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ATCC l paracasei atcc 25598
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ATCC lactobacillus reference strains
Specificity of the L. Casei Primer Pair Used in This Study
Lactobacillus Reference Strains, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC lacticaseibacillus paracasei atcc 25598
Specificity of the L. Casei Primer Pair Used in This Study
Lacticaseibacillus Paracasei Atcc 25598, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Specificity of the L. Casei Primer Pair Used in This Study
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Specificity of the L. Casei Primer Pair Used in This Study
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Specificity of the L. Casei Primer Pair Used in This Study
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Proteintech nfu1
Mechanism hypothesis diagram. Under normal conditions, transferrin receptor 1 (TFR1) on the cell membrane facilitates the uptake of iron from circulating iron ions and iron-bound transferrin into the cell, where it is reduced to ferrous iron (Fe 2+ ). Mitochondrial TFR1 (mTFR1) then transports Fe 2+ into the mitochondria, where it participates in the synthesis of [2Fe–2S] clusters, which are further assembled into [4Fe–4S] clusters with the mediation of ISCA1, ISCA2, and <t>NFU1.</t> These [4Fe–4S] clusters are inserted into the LIAS protein, enabling its interaction with GCSH and facilitating the lipoylation of mitochondrial proteins such as DLAT and DLST, which are essential for the TCA cycle and normal cellular respiration. In contrast, under ischemia-reperfusion conditions, the upregulation of TFR1 and mTFR1 increases iron uptake, while the downregulation of ferroportin (FPN) reduces iron efflux, leading to elevated intracellular and mitochondrial Fe 2+ levels. Concurrently, the decreased expression of ISCA1, ISCA2, and NFU1 disrupts [4Fe–4S] cluster assembly and stability, impairing LIAS-GCSH interaction and lipoylation. This results in incomplete lipoylation of DLAT and other proteins, some of which form toxic oligomers by binding to mitochondrial copper ions. Both non-lipoylated and oligomerized proteins fail to participate in the TCA cycle, ultimately leading to cell death.
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Mechanism hypothesis diagram. Under normal conditions, transferrin receptor 1 (TFR1) on the cell membrane facilitates the uptake of iron from circulating iron ions and iron-bound transferrin into the cell, where it is reduced to ferrous iron (Fe 2+ ). Mitochondrial TFR1 (mTFR1) then transports Fe 2+ into the mitochondria, where it participates in the synthesis of [2Fe–2S] clusters, which are further assembled into [4Fe–4S] clusters with the mediation of ISCA1, ISCA2, and <t>NFU1.</t> These [4Fe–4S] clusters are inserted into the LIAS protein, enabling its interaction with GCSH and facilitating the lipoylation of mitochondrial proteins such as DLAT and DLST, which are essential for the TCA cycle and normal cellular respiration. In contrast, under ischemia-reperfusion conditions, the upregulation of TFR1 and mTFR1 increases iron uptake, while the downregulation of ferroportin (FPN) reduces iron efflux, leading to elevated intracellular and mitochondrial Fe 2+ levels. Concurrently, the decreased expression of ISCA1, ISCA2, and NFU1 disrupts [4Fe–4S] cluster assembly and stability, impairing LIAS-GCSH interaction and lipoylation. This results in incomplete lipoylation of DLAT and other proteins, some of which form toxic oligomers by binding to mitochondrial copper ions. Both non-lipoylated and oligomerized proteins fail to participate in the TCA cycle, ultimately leading to cell death.
Cheryl Arrowsmith, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Specificity of the L. Casei Primer Pair Used in This Study

Journal: Clinical and Experimental Gastroenterology

Article Title: Quantification of Intestinal Lactobacillus Species in Children with Functional Constipation by Quantitative Real-Time PCR

doi: 10.2147/CEG.S250755

Figure Lengend Snippet: Specificity of the L. Casei Primer Pair Used in This Study

Article Snippet: Seven Lactobacillus reference strains ( L. casei ATCC 39392, L. paracasei ATCC 25598, L. rhamnosus ATCC 7469, L. plantarum ATCC 8014, L. reuteri ATCC 23272, L. fermentum ATCC 9338, L. acidophilus ATCC 4356) used to validate the assays in the study were ordered from the Iranian Research Organization for Science and Technology (IROST, Iran).

Techniques: Real-time Polymerase Chain Reaction

Prevalence of  Lactobacillus  Species, Detected by Quantitative PCR

Journal: Clinical and Experimental Gastroenterology

Article Title: Quantification of Intestinal Lactobacillus Species in Children with Functional Constipation by Quantitative Real-Time PCR

doi: 10.2147/CEG.S250755

Figure Lengend Snippet: Prevalence of Lactobacillus Species, Detected by Quantitative PCR

Article Snippet: Seven Lactobacillus reference strains ( L. casei ATCC 39392, L. paracasei ATCC 25598, L. rhamnosus ATCC 7469, L. plantarum ATCC 8014, L. reuteri ATCC 23272, L. fermentum ATCC 9338, L. acidophilus ATCC 4356) used to validate the assays in the study were ordered from the Iranian Research Organization for Science and Technology (IROST, Iran).

Techniques:

Quantity of seven Lactobacillus species in the feces of constipated children and healthy controls. Statistical significance of observed differences in the amount of Lactobacillus species between both constipated and healthy groups was measured by the Mann–Whitney U -test. Bars represent standard errors. P < 0.05 was marked with one asterisk (∗), and P < 0.2 with two asterisks (∗∗). One-way ANOVA testing shows the significant differences in quantity (log 10 CFU/gram) between Lactobacillus species.

Journal: Clinical and Experimental Gastroenterology

Article Title: Quantification of Intestinal Lactobacillus Species in Children with Functional Constipation by Quantitative Real-Time PCR

doi: 10.2147/CEG.S250755

Figure Lengend Snippet: Quantity of seven Lactobacillus species in the feces of constipated children and healthy controls. Statistical significance of observed differences in the amount of Lactobacillus species between both constipated and healthy groups was measured by the Mann–Whitney U -test. Bars represent standard errors. P < 0.05 was marked with one asterisk (∗), and P < 0.2 with two asterisks (∗∗). One-way ANOVA testing shows the significant differences in quantity (log 10 CFU/gram) between Lactobacillus species.

Article Snippet: Seven Lactobacillus reference strains ( L. casei ATCC 39392, L. paracasei ATCC 25598, L. rhamnosus ATCC 7469, L. plantarum ATCC 8014, L. reuteri ATCC 23272, L. fermentum ATCC 9338, L. acidophilus ATCC 4356) used to validate the assays in the study were ordered from the Iranian Research Organization for Science and Technology (IROST, Iran).

Techniques: MANN-WHITNEY

Mechanism hypothesis diagram. Under normal conditions, transferrin receptor 1 (TFR1) on the cell membrane facilitates the uptake of iron from circulating iron ions and iron-bound transferrin into the cell, where it is reduced to ferrous iron (Fe 2+ ). Mitochondrial TFR1 (mTFR1) then transports Fe 2+ into the mitochondria, where it participates in the synthesis of [2Fe–2S] clusters, which are further assembled into [4Fe–4S] clusters with the mediation of ISCA1, ISCA2, and NFU1. These [4Fe–4S] clusters are inserted into the LIAS protein, enabling its interaction with GCSH and facilitating the lipoylation of mitochondrial proteins such as DLAT and DLST, which are essential for the TCA cycle and normal cellular respiration. In contrast, under ischemia-reperfusion conditions, the upregulation of TFR1 and mTFR1 increases iron uptake, while the downregulation of ferroportin (FPN) reduces iron efflux, leading to elevated intracellular and mitochondrial Fe 2+ levels. Concurrently, the decreased expression of ISCA1, ISCA2, and NFU1 disrupts [4Fe–4S] cluster assembly and stability, impairing LIAS-GCSH interaction and lipoylation. This results in incomplete lipoylation of DLAT and other proteins, some of which form toxic oligomers by binding to mitochondrial copper ions. Both non-lipoylated and oligomerized proteins fail to participate in the TCA cycle, ultimately leading to cell death.

Journal: Redox Biology

Article Title: Iron overload exaggerates renal ischemia-reperfusion injury by promoting tubular cuproptosis via interrupting function of LIAS

doi: 10.1016/j.redox.2025.103795

Figure Lengend Snippet: Mechanism hypothesis diagram. Under normal conditions, transferrin receptor 1 (TFR1) on the cell membrane facilitates the uptake of iron from circulating iron ions and iron-bound transferrin into the cell, where it is reduced to ferrous iron (Fe 2+ ). Mitochondrial TFR1 (mTFR1) then transports Fe 2+ into the mitochondria, where it participates in the synthesis of [2Fe–2S] clusters, which are further assembled into [4Fe–4S] clusters with the mediation of ISCA1, ISCA2, and NFU1. These [4Fe–4S] clusters are inserted into the LIAS protein, enabling its interaction with GCSH and facilitating the lipoylation of mitochondrial proteins such as DLAT and DLST, which are essential for the TCA cycle and normal cellular respiration. In contrast, under ischemia-reperfusion conditions, the upregulation of TFR1 and mTFR1 increases iron uptake, while the downregulation of ferroportin (FPN) reduces iron efflux, leading to elevated intracellular and mitochondrial Fe 2+ levels. Concurrently, the decreased expression of ISCA1, ISCA2, and NFU1 disrupts [4Fe–4S] cluster assembly and stability, impairing LIAS-GCSH interaction and lipoylation. This results in incomplete lipoylation of DLAT and other proteins, some of which form toxic oligomers by binding to mitochondrial copper ions. Both non-lipoylated and oligomerized proteins fail to participate in the TCA cycle, ultimately leading to cell death.

Article Snippet: Membranes were blocked with 5 % non-fat milk and incubated overnight at 4 °C with primary antibodies against: DLAT (Proteintech, 68303-1-Ig, 1:5000), HSP70 (Proteintech, 10995-1-AP, 1:5000), SDHB (Proteintech, 10620-1-AP, 1:5000), GCSH (Proteintech, 16726-1-AP, 1:500), SLC40A1 (Proteintech, 26601-1-AP, 1:100), α-Tublin (Proteintech, 14555-1-AP, 1:5000), ISCA2 (Proteintech, 13200-1-AP, 1:1000), ATP5A1 (Proteintech, 66037-1-Ig, 1:5000), COX-1 (Proteintech, 13393-1-AP, 1:500), NFU1 (Proteintech, 25598-1-AP, 1:500), 6∗His (Proteintech, 66005-1-Ig, 1:5000), GST (Proteintech, 66001-2-Ig, 1:5000), LIAS (Proteintech, 11577-1-AP, 1:1000), GPX4 (Abcam, ab252833, 1:1000), Anti-Lipoic Acid Rabbit pAb (Millipore, 437695, 1:1000).

Techniques: Membrane, Expressing, Binding Assay