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spc 400  (StressMarq)


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    StressMarq spc 400
    Spc 400, supplied by StressMarq, used in various techniques. Bioz Stars score: 93/100, based on 43 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/spc 400/product/StressMarq
    Average 93 stars, based on 43 article reviews
    spc 400 - by Bioz Stars, 2026-02
    93/100 stars

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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and <t>NHE3</t> and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.
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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and <t>NHE3</t> and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.
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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and <t>NHE3</t> and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.
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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and <t>NHE3</t> and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.
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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and <t>NHE3</t> and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.
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    nkcc2  (StressMarq)
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    StressMarq nkcc2
    Expression of key proteins involved in renal calcium, magnesium, and salt handling. Protein abundance was assessed by immunoblotting in protein homogenates from kidneys from wildtype (WT/WT), Pth KO/ Casr BCH002 , WT/ Casr BCH002 and Pth KO/ Casr BCH002 mice. Protein expression of ( A , B ) <t>NKCC2</t> (120 kDa), ( C , D ) NCC (130 kDa), ( E , F ) TRPV5 (75 kDa) ( G , H ) Calbindin D28k (28 kDa), and ( I , J ) TRPM6 (230 kDa) were normalized to the corresponding ponceau S staining. Values are presented as means ± SD together with single values ( n = 6/group). Data were analysed with 2-way ANOVA with Tukey correction for multiple comparisons between PTH and BCH genotypes. * p < 0.05
    Nkcc2, supplied by StressMarq, 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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    K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and NHE3 and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.

    Journal: iScience

    Article Title: K ir 5.1-modulated potassium flux stimulates an anabolic kidney phenotype

    doi: 10.1016/j.isci.2025.113601

    Figure Lengend Snippet: K ir 5.1 DN animals fail to mount an adequate physiological response to dietary K + depletion (A–C) K ir 5.1 DN mice had increased urine K + concentrations, B) urine K + excretions, and C) cumulative urine K + losses compared with K ir 5.1 WT controls on a K + -free diet. (D and E) Urine Na + D) concentrations and E) excretions did not differ between genotypes. (F–J) K ir 5.1 DN mice had increased urine Na + -to-K + ratios under K + -free conditions. After consuming a K + -free diet for four days, K ir 5.1 DN mice had G) unchanged blood Na + , H) reduced blood K + , I) unchanged blood Cl − , and J) reduced blood HCO 3 − relative to K ir 5.1 WT controls. Note, K + values in the K ir 5.1 DN group were at the lower limit of detection. A nonparametric analysis was performed for K + , given the lack of normality. (K) Urine K + excretion in two groups of K ir 5.1 DN animals. One group was treated with a K + -free diet alone, while the other group was additionally treated with the ENaC inhibitor, triamterene. (L) Kidney Western blot data after the consumption of a K + -free diet for four days. Compared with K ir 5.1 WT controls, K ir 5.1 DN mice had reduced abundances of NBCe1 and NHE3 and increased NKCC2 abundance. Abundances of pNCC and total NCC trended toward being reduced, but did not achieve the threshold for statistical significance. Ponceau shown for pNCC and NHE3. Ponceaus for NBCe1, NKCC2, and tNCC included as . N = 5 and 7 for A-F. N = 10 and 8 for G-J. N = 4 per group for K. N = 5 per group for L. # indicates p < 0.05 by two-way ANOVA with repeated measures followed by Sidak’s post-hoc test. † indicates p < 0.05 for interaction by two-way ANOVA with repeated measures. ∗ indicates p < 0.05 by two-tailed Student’s unpaired t-test (or Mann-Whitney for H). Data are mean +/− SEM.

    Article Snippet: NHE3 , Stressmarq , SPC-400.

    Techniques: Western Blot, Two Tailed Test, MANN-WHITNEY

    Expression of key proteins involved in renal calcium, magnesium, and salt handling. Protein abundance was assessed by immunoblotting in protein homogenates from kidneys from wildtype (WT/WT), Pth KO/ Casr BCH002 , WT/ Casr BCH002 and Pth KO/ Casr BCH002 mice. Protein expression of ( A , B ) NKCC2 (120 kDa), ( C , D ) NCC (130 kDa), ( E , F ) TRPV5 (75 kDa) ( G , H ) Calbindin D28k (28 kDa), and ( I , J ) TRPM6 (230 kDa) were normalized to the corresponding ponceau S staining. Values are presented as means ± SD together with single values ( n = 6/group). Data were analysed with 2-way ANOVA with Tukey correction for multiple comparisons between PTH and BCH genotypes. * p < 0.05

    Journal: Pflugers Archiv

    Article Title: A novel mouse model for familial hypocalciuric hypercalcemia (FHH1) reveals PTH-dependent and independent CaSR defects

    doi: 10.1007/s00424-024-02927-y

    Figure Lengend Snippet: Expression of key proteins involved in renal calcium, magnesium, and salt handling. Protein abundance was assessed by immunoblotting in protein homogenates from kidneys from wildtype (WT/WT), Pth KO/ Casr BCH002 , WT/ Casr BCH002 and Pth KO/ Casr BCH002 mice. Protein expression of ( A , B ) NKCC2 (120 kDa), ( C , D ) NCC (130 kDa), ( E , F ) TRPV5 (75 kDa) ( G , H ) Calbindin D28k (28 kDa), and ( I , J ) TRPM6 (230 kDa) were normalized to the corresponding ponceau S staining. Values are presented as means ± SD together with single values ( n = 6/group). Data were analysed with 2-way ANOVA with Tukey correction for multiple comparisons between PTH and BCH genotypes. * p < 0.05

    Article Snippet: Antibodies used were directed against NaPi-IIa (1:2000) [ ], NaPi-IIc (1:1000) [ ], total NCC (1:2000; a kind gift of J. Loffing [ ]), NKCC2 (1:2000, a kind gift of J. Loffing) [ ], NHE3 (1:1000; StressMarq; SPC-400D), TRPV5 (1: 500, a kind gift by O. Bonny, [ ]), TRPM6 (1:2000, a kind gift by J. Loffing, [ ]), the vitamin D receptor (Vdr) (1:500 Santa Cruz), Cyp24a1 (1:1000, Proteintech), the Ca 2+ -sensing receptor (CaSR) (1:500, Thermo Fisher) and calbindin D28k (1:500, Swant).

    Techniques: Expressing, Western Blot, Staining