Journal: Internal medicine (Tokyo, Japan)

Article Title: Decreased Renal Expression of H(+)-ATPase and Pendrin in a Patient with Distal Renal Tubular Acidosis Associated with Sjögren's Syndrome.

doi: 10.2169/internalmedicine.54.4821

Figure Lengend Snippet: Figure 3. Double-labeling immunofluorescence histochemical staining showed similar labeling pat- terns for pendrin in the control and the Sjögren’s syndrome patient, but there was a distinct red fluo- rescence in the normal kidney, whereas the Sjögren’s syndrome patient’s specimen revealed a weak red fluorescence of H+-ATPase and pendrin. A: Control, AQP2+DAPI, B: Control, Pendrin+DAPI, C: Control, merge, D: Patient, AQP2+DAPI, E: Patient, Pendrin+DAPI, F: Patient, merge. AQP2: Aquaporin 2, DAPI: 4’,6-diamidino-2-phenylindole nuclear stain

Article Snippet: After washing in PBS, the slides were incubated with anti-vacuolar-type H+-ATPase antibody (rabbit anti-human, 1:2,000; Santa Cruz Biotechnology) or anti-pendrin antibody (mouse anti-human, 1:500; Acris antibodies, San Diego, USA) at 4°C overnight.

Techniques: Labeling, Immunofluorescence, Staining, Control, Fluorescence

Journal: Journal of Translational Medicine

Article Title: SLC26A4 correlates with homologous recombination deficiency and patient prognosis in prostate cancer

doi: 10.1186/s12967-022-03513-5

Figure Lengend Snippet: The results of multi-omics analysis of SLC26A4. A Correlations between SLC26A4 expression and abundances of immune cells, including CD4 naïve T cell, exhausted T cell, Th1, and Th2 cell. B Kaplan–Meier survival plots of SLC26A4 in TCGA-PRAD, MSKCC, and GSE116918 cohorts. C Forest plot of meta-analysis integrating SLC26A4’s role in these three datasets. D Expression levels of SLC26A4 between normal and tumor tissues in pan-cancer. E Correlations between SLC26A4 and survival in pan-cancer. F Correlations between SLC26A4 expression and functional states at the single-cell level. G Correlations between SLC26A4 expression and methylation. The statistical significance is indicated as asterisks (*), *p < 0.05, ** p < 0.01, ***p < 0.001, ns: not significant

Article Snippet: These paraffin-embedded tissues were sectioned (4 μm) and stained with antibodies against SLC26A4 (HPA042860, Atlas Antibodies).

Techniques: Biomarker Discovery, Expressing, Functional Assay, Methylation

Journal: Journal of Translational Medicine

Article Title: SLC26A4 correlates with homologous recombination deficiency and patient prognosis in prostate cancer

doi: 10.1186/s12967-022-03513-5

Figure Lengend Snippet: Validation of SLC26A4 in Xiangya cohort. A Expression difference of SLC26A4 mRNA and IHC between PCa and BPH tissues. B ROC curves of age, baseline PSA, and SLC26A4 mRNA and IHC in distinguishing PCa and BPH samples. C Expression difference of SLC26A4 mRNA and IHC between HRD and non-HRD PCa tissues. D ROC curves of age, Gleason score, baseline PSA, and SLC26A4 mRNA and IHC in distinguishing HRD and non-HRD PCa samples. Representative immunohistochemical results of E BPH, F HRD PCa, and G non-HRD PCa samples

Article Snippet: These paraffin-embedded tissues were sectioned (4 μm) and stained with antibodies against SLC26A4 (HPA042860, Atlas Antibodies).

Techniques: Biomarker Discovery, Expressing, Immunohistochemical staining

Journal: Frontiers in medicine

Article Title: Urinary Extracellular Vesicles for Renal Tubular Transporters Expression in Patients With Gitelman Syndrome.

doi: 10.3389/fmed.2021.679171

Figure Lengend Snippet: FIGURE 1 | Characterization of urinary extracellular vesicles (uEVs) from healthy controls. (A) Screen shot from 1:2,000 diluted urine sample reveals a range of particle sizes by nanoparticle tracking analysis (NTA). (B) Concentration and size distribution of uEVs (0–150 nm diameter) by NTA were shown. The concentration is expressed as number of particles per ml. (C) uEVs particles were correlated strongly with urine creatinine (r2 for 0.81, P < 0.0001). (D) Transmission electron microscopy of uEVs was shown (scale bar 100 nm). (E) uEVs markers (AQP2, TSG101, NSE, and CD9) were assessed by immunoblotting. (F) Expression pattern of renal transporters including NHE3, NKCC2, NCC, p-NCC, ENaCβ, pendrin, ROMK, and Maxi-K from healthy controls was similar.

Article Snippet: The primary antibodies were as follows: NSE (ab254088, Abcam, Cambridge, UK), TSG101 (ab125011, Abcam, Cambridge, UK), CD9 (GTX55564, Genetex, HsinChu City), AQP2 (sc-515770, Santa Cruz Biotechnology, Santa Cruz, CA), NHE3 (NHE31-A, Alpha Diagnostic Intl Inc., San Antonio, TX) (6), NKCC2 (AB2281, Millipore, Temecula, CA), NCC (AB3553, Millipore, Temecula, CA) (23), ENaCβ (ASC-019, Alomone labs, Jerusalem, Israel) (23), p-NCC (17T, in-house antibody) (23), Maxi-K (APC-021, Alomone labs, Jerusalem, Israel) (6), ROMK (APC-001, Alomone labs, Jerusalem, Israel) (6), and pendrin (ARP41739_P050, Aviva system biology, San Diego, CA).

Techniques: Concentration Assay, Transmission Assay, Electron Microscopy, Western Blot, Expressing

Journal: Frontiers in medicine

Article Title: Urinary Extracellular Vesicles for Renal Tubular Transporters Expression in Patients With Gitelman Syndrome.

doi: 10.3389/fmed.2021.679171

Figure Lengend Snippet: FIGURE 2 | Renal Na+ and K+ associated transporters expression from urinary extracellular vesicles in patients with GS (n = 10) compared with healthy controls. (A) Immunoblotting of renal transporters (NHE3, NKCC2, NCC, p-NCC, ENaCβ, pendrin, ROMK, Maxi-K, and CD9). (B) Quantification of immunoblotting of NHE3, NKCC2, NCC, p-NCC, ENaCβ, pendrin, ROMK, Maxi-K, and CD9. Error bars, standard deviation. *P < 0.05, **P < 0.01.

Article Snippet: The primary antibodies were as follows: NSE (ab254088, Abcam, Cambridge, UK), TSG101 (ab125011, Abcam, Cambridge, UK), CD9 (GTX55564, Genetex, HsinChu City), AQP2 (sc-515770, Santa Cruz Biotechnology, Santa Cruz, CA), NHE3 (NHE31-A, Alpha Diagnostic Intl Inc., San Antonio, TX) (6), NKCC2 (AB2281, Millipore, Temecula, CA), NCC (AB3553, Millipore, Temecula, CA) (23), ENaCβ (ASC-019, Alomone labs, Jerusalem, Israel) (23), p-NCC (17T, in-house antibody) (23), Maxi-K (APC-021, Alomone labs, Jerusalem, Israel) (6), ROMK (APC-001, Alomone labs, Jerusalem, Israel) (6), and pendrin (ARP41739_P050, Aviva system biology, San Diego, CA).

Techniques: Expressing, Western Blot, Standard Deviation

Journal: Frontiers in medicine

Article Title: Urinary Extracellular Vesicles for Renal Tubular Transporters Expression in Patients With Gitelman Syndrome.

doi: 10.3389/fmed.2021.679171

Figure Lengend Snippet: FIGURE 3 | Immunofluorescence of biopsied kidney tissues from another 3 representative GS patients (GS 1, GS 2, and GS 3) compared with the control kidney tissue. Renal transporters including NHE3, NKCC2, NCC, p-NCC, ENaCβ, pendrin, ROMK, Maxi-K were stained with green. AQP2 was stained with red for localization. Scale bar, 50 µm.

Article Snippet: The primary antibodies were as follows: NSE (ab254088, Abcam, Cambridge, UK), TSG101 (ab125011, Abcam, Cambridge, UK), CD9 (GTX55564, Genetex, HsinChu City), AQP2 (sc-515770, Santa Cruz Biotechnology, Santa Cruz, CA), NHE3 (NHE31-A, Alpha Diagnostic Intl Inc., San Antonio, TX) (6), NKCC2 (AB2281, Millipore, Temecula, CA), NCC (AB3553, Millipore, Temecula, CA) (23), ENaCβ (ASC-019, Alomone labs, Jerusalem, Israel) (23), p-NCC (17T, in-house antibody) (23), Maxi-K (APC-021, Alomone labs, Jerusalem, Israel) (6), ROMK (APC-001, Alomone labs, Jerusalem, Israel) (6), and pendrin (ARP41739_P050, Aviva system biology, San Diego, CA).

Techniques: Control, Staining

Journal: Frontiers in medicine

Article Title: Urinary Extracellular Vesicles for Renal Tubular Transporters Expression in Patients With Gitelman Syndrome.

doi: 10.3389/fmed.2021.679171

Figure Lengend Snippet: FIGURE 4 | Renal transporters expression from urinary extracellular vesicles (uEVs) and immunofluorescence of biopsied kidney tissues from bulimic patients. (A) Immunoblotting of renal transporters (NHE3, NKCC2, NCC, p-NCC, ENaCβ, pendrin, ROMK, Maxi-K, and CD9) from uEVs in bulimic patients (n = 3) compared with healthy control. (B) Immunofluorescence of NHE3, NKCC2, NCC, p-NCC (green, right) and ENaCβ, pendrin, ROMK, Maxi-K (green, left) from one representative bulimia patient compared with the control. AQP2 was stained with red for localization. Scale bar, 50 µm.

Article Snippet: The primary antibodies were as follows: NSE (ab254088, Abcam, Cambridge, UK), TSG101 (ab125011, Abcam, Cambridge, UK), CD9 (GTX55564, Genetex, HsinChu City), AQP2 (sc-515770, Santa Cruz Biotechnology, Santa Cruz, CA), NHE3 (NHE31-A, Alpha Diagnostic Intl Inc., San Antonio, TX) (6), NKCC2 (AB2281, Millipore, Temecula, CA), NCC (AB3553, Millipore, Temecula, CA) (23), ENaCβ (ASC-019, Alomone labs, Jerusalem, Israel) (23), p-NCC (17T, in-house antibody) (23), Maxi-K (APC-021, Alomone labs, Jerusalem, Israel) (6), ROMK (APC-001, Alomone labs, Jerusalem, Israel) (6), and pendrin (ARP41739_P050, Aviva system biology, San Diego, CA).

Techniques: Expressing, Western Blot, Control, Staining

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: Pendrin expression and generation of pendrin knockdown (PDS‐KD) Calu‐3 cell lines. (A) CFTR, SLC26A4, SLC26A6, and SLC26A9 mRNA expression in Scr‐KD (control) and PDS‐KD (pendrin knockdown) cells. mRNA levels were measured using qRT‐PCR, normalized to GAPDH, and plotted relative to the corresponding value in parental Calu‐3 cells. PDS mRNA expression was unchanged in Scr‐KD cells and was reduced ~90% in the PDS‐KD line transduced with sh‐PDS‐5 ( n = 5, P < 0.0001). CFTR, SCL26A6, and A9 mRNA levels were not altered significantly in pendrin knockdown cells. (B) (i) immunstaining ZO‐1 (red) and pendrin (green) in parental Calu‐3 (WT) cells, (ii) same as (i) but omitting antipendrin primary antibody, panels (iii)–(vi) pendrin immunostaining in WT cells, scrambled control shRNA cells, CFTR knockdown cells, and pendrin knockdown cells, respectively. All images were taken using the same illumination intensity and laser power. Scale bars: 20 μ m. Images are representative of n = 4–5 cultures/cell line. (C) summary of pendrin fluorescence intensity in parental (WT), Scr‐KD (shRNA scrambled control cells), PDS‐KD (pendrin knockdown cells) and CFTR‐KD cells (CFTR knockdown cells, n = 4–5, ± SEM). Pendrin staining was reduced ~80% in PDS‐KD compared to parental and scrambled shRNA control cells. Unpaired Student's t tests show * P < 0.05, ** P < 0.01, *** P < 0.001. (D–G) immunoblots of Calu‐3 parental, Scr‐KD, and PDS‐KD cells. 20 μ g total protein was probed with antibody against: (D) AE2 and Na + /K + ‐ATPase α ‐subunit; (E) CFTR and Na + /K + ‐ATPase a‐subunit; (F) NBCe1 and β ‐actin, and (G) NKCC1 and Na + /K + ‐ATPase α ‐subunit. (H) summary of expression of different transporters in parental, scrambled shRNA control, and pendrin knockdown cell lines. Each protein was corrected for loading using β ‐actin or Na + /K + ‐ATPase, and normalized to the expression in parental Calu‐3 cells.

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Expressing, Knockdown, Control, Quantitative RT-PCR, Transduction, Immunostaining, shRNA, Fluorescence, Staining, Western Blot

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: Pendrin knockdown does not affect forskolin‐stimulated HCO 3 − secretion under open‐circuit, pH stat conditions. Forskolin and CFTR Inh ‐172 were added sequentially to the basolateral and apical sides, respectively. I eq (blue symbols) and HCO 3 − secretion (red symbols) were monitored across (A) Scr‐KD, and (B) PDS‐KD monolayers. (C) net HCO 3 − secretion rates. There was no difference in forskolin‐stimulated or residual HCO 3 − ‐secretion rates after CFTR Inh ‐172 when comparing Scr‐KD and PDS‐KD cells (mean ± SEM, n = 4–9; * P < 0.05).

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Knockdown

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: No evidence for pendrin‐dependent, apical Cl − /HCO 3 − exchange in basolaterally permeabilized Calu‐3 monolayers. (A–C) cultures were bathed initially in symmetrical Cl − ‐free solutions and permeabilized basolaterally using nystatin (360 μ g·mL −1 ). Apical HCO 3 − efflux was monitored using pH stat. 30 mmol/L NaCl was added on the apical side to establish an apical‐to‐basolateral Cl − gradient and 10 μ mol/L forskolin was added to stimulate CFTR. (D) summary of HCO 3 − secretion rates under each condition (mean ± SEM, n = 4–9). HCO 3 − secretion by Calu‐3 Scr‐KD and PDS‐KD monolayers was negligible in unstimulated monolayers with Cl − gradient, and similar after forskolin addition (ns, not significant, P > 0.2).

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques:

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: Anion exchange in cAMP‐stimulated Calu‐3 monolayers exposed to basolateral H 2 DIDS and apical CFTR inh ‐172. Polarized cells were superfused with HCO 3 − ‐buffered solution and apical Cl − was replaced with gluconate during stimulation with 10 μ mol/L forskolin and exposure to basolateral 500 μ mol/L H 2 DIDS as indicated. Continuous traces show the mean pH i and the dashed lines indicate ± SEM, n = 4–7. (A) SCR‐KD (control) cells, (B) Pendrin‐KD cells, (C) CFTR‐KD cells, and (D) AE2‐ KD cells. (I) summary of alterations in pH i induced by apical Cl − substitution using parental (WT) Calu‐3 cells that had been cultured under air–liquid interface (ALI) or submerged (Sub) conditions and exposed acutely to CFTR inhibitors on the apical side and to basolateral H 2 DIDS to minimize HCO 3 − flux through non‐pendrin transporters. Also shown are the responses to apical Cl − substitution together with basolateral H 2 DIDS from experiments in (A–D) using Scr‐KD (control) and knockdown cell lines deficient in PDS, CFTR, and AE2.

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Control, Cell Culture, Knockdown

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: Effects of altering apical HCO 3 − concentration on pH i in control, pendrin knockdown, and CFTR knockdown Calu‐3 cell lines. (A) intracellular pH was measured in Scr‐KD, PDS‐KD, and CFTR‐KD monolayers bathed basolaterally with HCO 3 − ‐buffered solution (25 mmol/L) and H 2 ‐DIDS, and challenged with the apical [HCO 3 − ] shown. Recordings on the left were obtained without forskolin stimulation, those on the right with forskolin. Also shown with red dashed lines are the mean responses when 10 μ mol/L CFTR inh ‐172 was added to assess the dependence on CFTR under these conditions. (B) summary of pH i changes in stimulated cells induced by exposure to high apical [HCO 3 − ] (50 mmol/L) in the absence (−) or presence (+) of CFTR inh ‐172 (mean ± SEM, n = 4; *** P < 0.001).

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Concentration Assay, Control, Knockdown

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: IL‐4 effects on pendrin expression in Calu‐3 cells, fluid secretion rate, and pH of secretions. (A) relative pendrin mRNA expression in cell lines measured using quantitative real‐time PCR and normalized to GAPDH after 48 h treatment with IL‐4 (10 ng/mL) at the air–liquid interface. (B) background‐subtracted images of parental (WT) and pendrin knockdown (PDS‐KD) cells immunostained for pendrin with or without 48 h pretreatment with IL‐4 (10 ng/mL). (C) summary of image fluorescence intensities in arbitrary units (A.U.). ns, not significant. ( P > 0.05). Pendrin protein staining was not increased significantly in Calu‐3 cells treated with IL‐4. (D) cumulative fluid secretion after 2 day pretreatment with DMSO (vehicle) or IL‐4 (10 ng/mL). Fluid was collected at 24 h intervals. cAMP + forskolin (C+F; or vehicle control) was added in some experiments to activate CFTR. (E and F) pH of the fluid secreted in panels (C) 0–24 h, and (D) 24–48 h, respectively.

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Expressing, Real-time Polymerase Chain Reaction, Knockdown, Fluorescence, Staining, Control

Journal: Physiological Reports

Article Title: Most bicarbonate secretion by Calu‐3 cells is mediated by CFTR and independent of pendrin

doi: 10.14814/phy2.13641

Figure Lengend Snippet: Comparison of CFTR, pendrin, SLC26A6, and SLC26A9 expression in cultures at the air–liquid interface (ALI) versus submerged conditions. qRT‐PCR was performed using (A) Scr‐KD (control) cells, (B) PDS‐KD, and (C) parental cells (WT), normalized to the levels in ALI cultures. (mean ± SEM, n = 3–5; * P < 0.05, ** P < 0.01, one‐tailed Student's t test). (D) comparison of qRT‐PCR results for the four genes examined, each normalized to GAPDH expression, showing relative levels of CFTR and SLC26A transporters. (E) relative expression of SLC26A transporters, rescaled to enable comparison. Note that after normalization to GAPDH, the qRT‐PCR signals for SLC26A6 and SLC26A9 were >100‐fold higher than for pendrin.

Article Snippet: Taqman primers (Life technologies; Assay ID: CFTR: Hs00357011_m1; SLC26A4: Hs01070620_m1; SLC26A6: Hs00370470_m1; SLC26A9: Hs00369451_m1) and the QuantStudioTM 7 Flex Real‐Time PCR system (Life Technologies) were used. qRT‐PCR was performed using the “Fast” program: 95°C for 20 sec, followed by 40 cycles of 95°C for 1 sec and 60°C for 20 sec. Data were normalized to GAPDH.

Techniques: Comparison, Expressing, Quantitative RT-PCR, Control, One-tailed Test

Journal: Medical Principles and Practice

Article Title: Iodide Transporters in the Endometrium: A Potential Diagnostic Marker for Women with Recurrent Pregnancy Failures

doi: 10.1159/000508309

Figure Lengend Snippet: Endometrial biopsies from women with RPF express higher transcript levels of NIS and PENDRIN. Mid-luteal phase endometrial biopsy tissue was obtained from patients (RPF) or control biopsies. Leukocytes were obtained from peripheral blood of healthy volunteers. a DNA gel electrophoresis from amplified RT-PCR products representing 4 controls (c1–c4) and 8 patient (p1–p8) biopsies. b Quantitative RT-PCR: normalized gene expression (to internal B2M) comparing control and RPF groups along with leukocytes represented as mean ± SEM. NIS RPF n = 57, PENDRIN RPF n = 60, TG RPF n = 40. *p < 0.05. NS, not significant.

Article Snippet: The following validated Taqman primers and probe were obtained from Invitrogen: NIS: Hs00950365_m1, PENDRIN: Hs01070627_m1, TG: Hs00174974_m1, B2M: Hs00187842_m1.

Techniques: Control, DNA Gel Electrophoresis, Amplification, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Gene Expression

Journal: Medical Principles and Practice

Article Title: Iodide Transporters in the Endometrium: A Potential Diagnostic Marker for Women with Recurrent Pregnancy Failures

doi: 10.1159/000508309

Figure Lengend Snippet: Targeted RNASeq analysis of endometrial biopsies. Endometrial biopsy tissue was obtained from 42 more patients not utilized in q-RTPCR analysis. a Quantified expression from RNASeq analysis for one control gene (B2M) and NIS and PENDRIN represented as mean ± SEM. RPF n = 42. b Heatmap analysis was created utilizing “Morpheus” software. *p < 0.05, **p < 0.005. NS, not significant.

Article Snippet: The following validated Taqman primers and probe were obtained from Invitrogen: NIS: Hs00950365_m1, PENDRIN: Hs01070627_m1, TG: Hs00174974_m1, B2M: Hs00187842_m1.

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Control, Software