scholarly journals Increased TPSAB1 Copy Number in a Family With Elevated Basal Serum Levels of Tryptase

2021 ◽  
Vol 8 ◽  
Author(s):  
Laura Hernández-Hernández ◽  
Catalina Sanz ◽  
Elena Marcos-Vadillo ◽  
Asunción García-Sánchez ◽  
Esther Moreno ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Copy Number ◽  
Family Members ◽  
Copy Number Gain ◽  
Digital Pcr ◽  
Gene Dose ◽  
Control Subjects ◽  
Basal Serum ◽  
The Family

Background: Some recent familial studies have described a pattern of autosomal dominant inheritance for increased basal serum tryptase (BST), but no correlation with mRNA expression and gene dose have been reported.Objective: We analyzed TPSAB1 mRNA expression and gene dose in a four-member family with high BST and in two control subjects.Methods: Blood samples were collected from the family and control subjects. Complete morphologic, immunophenotypical, and molecular bone marrow mast cell (MC) studies were performed. mRNA gene expression and gene dose were performed in a LightCycler 480 instrument. Genotype and CNV were performed by quantitative real-time digital PCR (qdPCR).Results: CNV analysis revealed a hereditary copy number gain genotype (3β2α) present in all the family members studied. The elevated total BST in the family members correlated with a significant increase in tryptase gene expression and dose.Conclusions and Clinical Relevance: We present a family with hereditary α-tryptasemia and elevated BST which correlated with a high expression of tryptase genes and an increased gene dose. The family members presented with atypical MC-mediator release symptoms or were even asymptomatic. Clinicians should be aware that elevated BST does not always mean an MC disorder.

scholarly journals Detection of Urinary Exosomal HSD11B2 mRNA Expression: A Useful Novel Tool for the Diagnostic Approach of Dysfunctional 11β-HSD2-Related Hypertension

2021 ◽  
Vol 12 ◽  
Author(s):  
Domenica De Santis ◽  
Annalisa Castagna ◽  
Elisa Danese ◽  
Silvia Udali ◽  
Nicola Martinelli ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Copy Number ◽  
Family Members ◽  
Digital Pcr ◽  
Regulatory Function ◽  
Compensatory Mechanism ◽  
Mrna Levels ◽  
Urinary Cortisol ◽  
Homozygous Mutant ◽  
Urinary Exosomes

ObjectiveApparent mineralocorticoid excess (AME) is an autosomal recessive disorder caused by the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) enzyme deficiency, traditionally assessed by measuring either the urinary cortisol metabolites ratio (tetrahydrocortisol+allotetrahydrocortisol/tetrahydrocortisone, THF+5αTHF/THE) or the urinary cortisol/cortisone (F/E) ratio. Exosomal mRNA is an emerging diagnostic tool due to its stability in body fluids and its biological regulatory function. It is unknown whether urinary exosomal HSD11B2 mRNA is related to steroid ratio or the HSD11B2 662 C>G genotype (corresponding to a 221 A>G substitution) in patients with AME and essential hypertension (EH).Aim of the StudyTo detect and quantify HSD11B2 mRNA from urinary exosomes in samples from family members affected by AME and EH, and to evaluate the relationship between exosomal HSD11B2 mRNA, steroid ratio, 662C>G genotype, and hypertension.MethodsIn this observational case–control study, urinary steroid ratios and biochemical parameters were measured. Urinary exosomes were extracted from urine and exosomal HSD11B2 mRNA was quantified by Droplet Digital PCR (ddPCR). B2M (β-2 microglobulin) gene was selected as the reference housekeeping gene.ResultsAmong family members affected by AME, exosomal urinary HSD11B2 mRNA expression was strictly related to genotypes. The two homozygous mutant probands showed the highest HSD11B2 mRNA levels (median 169, range 118–220 copies/µl) that progressively decreased in 221 AG heterozygous with hypertension (108, range 92–124 copies/µl), 221 AG heterozygous normotensives (23.35, range 8–38.7 copies/µl), and wild-type 221 AA subjects (5.5, range 4.5–14 copies/µl). Heterozygous hypertensive subjects had more HSD11B2 mRNA than heterozygous normotensive subjects. The F/E urinary ratio correlated with HSD11B2 mRNA copy number (p < 0.05); HSD11B2 mRNA strongly decreased while THF+5αTHF/THE increased in the two probands after therapy. In the AME family, HSD11B2 copy number correlated with both F/E and THF+5αTHF/THE ratios, whereas in EH patients, a high F/E ratio reflected a reduced HSD11B2 mRNA expression.ConclusionsHSD11B2 mRNA is detectable and quantifiable in urinary exosomes; its expression varies according to the 662 C>G genotype with the highest levels in homozygous mutant subjects. The HSD11B2 mRNA overexpression in AME could be due to a compensatory mechanism of the enzyme impairment. Exosomal mRNA is a useful tool to investigate HSD11B2 dysregulation in hypertension.

scholarly journals Clinical Importance of Myc Family Oncogene Aberrations in Epithelial Ovarian Cancer

2018 ◽  
Vol 2 (3) ◽  
Author(s):  
MoonSun Jung ◽  
Amanda J Russell ◽  
Catherine Kennedy ◽  
Andrew J Gifford ◽  
Kylie-Ann Mallitt ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Mrna Expression ◽  
Clinical Significance ◽  
Copy Number ◽  
Family Members ◽  
Activity Score ◽  
Gene Copy ◽  
Myc Oncogene ◽  
Statistical Algorithm

Abstract Background The Myc oncogene family has been implicated in many human malignancies and is often associated with particularly aggressive disease, suggesting Myc as an attractive prognostic marker and therapeutic target. However, for epithelial ovarian cancer (EOC), there is little consensus on the incidence and clinical relevance of Myc aberrations. Here we comprehensively investigated alterations in gene copy number, expression, and activity for Myc and evaluated their clinical significance in EOC. Methods To address inconsistencies in the literature regarding the definition of copy number variations, we developed a novel approach using quantitative polymerase chain reaction (qPCR) coupled with a statistical algorithm to estimate objective thresholds for detecting Myc gain/amplification in large cohorts of serous (n = 150) and endometrioid (n = 80) EOC. MYC, MYCN, and MYCL1 mRNA expression and Myc activity score for each case were examined by qPCR. Kaplan–Meier and Cox-regression analyses were conducted to assess clinical significance of Myc aberrations. Results Using a large panel of cancer cell lines (n = 34), we validated the statistical algorithm for determining clear thresholds for Myc gain/amplification. MYC was the most predominantly amplified of the Myc oncogene family members, and high MYC mRNA expression levels were associated with amplification in EOC. However, there was no association between prognosis and increased copy number or gene expression of MYC/MYCN/MYCL1 or with a pan-Myc transcriptional activity score, in EOC, although MYC amplification was associated with late stage and high grade in endometrioid EOC. Conclusion A systematic and comprehensive analysis of Myc genes, transcripts, and activity levels using qPCR revealed that although such aberrations commonly occur in EOC, overall they have limited impact on outcome, suggesting that the biological relevance of Myc oncogene family members is limited to certain subsets of this disease.

Quantitative analysis of CKS1B mRNA expression and copy number gain in patients with plasma cell disorders

2014 ◽  
Vol 53 (3) ◽  
pp. 110-117 ◽  
Author(s):  
Flavia Stella ◽  
Estela Pedrazzini ◽  
Edgardo Baialardo ◽  
Dorotea Beatriz Fantl ◽  
Natalia Schutz ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Mrna Expression ◽  
Plasma Cell ◽  
Copy Number ◽  
Copy Number Gain ◽  
Plasma Cell Disorders

scholarly journals S100 Calcium Binding Protein Family Members Associate With Poor Patient Outcome and Response to Proteasome Inhibition in Multiple Myeloma

2021 ◽  
Vol 9 ◽  
Author(s):  
Minxia Liu ◽  
Yinyin Wang ◽  
Juho J. Miettinen ◽  
Romika Kumari ◽  
Muntasir Mamun Majumder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Calcium Binding ◽  
Copy Number ◽  
Drug Response ◽  
Patient Survival ◽  
Family Members ◽  
Proteasome Inhibitors ◽  
S100 Family ◽  
Poor Patient ◽  
S100 Gene

Despite several new therapeutic options, multiple myeloma (MM) patients experience multiple relapses and inevitably become refractory to treatment. Insights into drug resistance mechanisms may lead to the development of novel treatment strategies. The S100 family is comprised of 21 calcium binding protein members with 17 S100 genes located in the 1q21 region, which is commonly amplified in MM. Dysregulated expression of S100 family members is associated with tumor initiation, progression and inflammation. However, the relationship between the S100 family and MM pathogenesis and drug response is unknown. In this study, the roles of S100 members were systematically studied at the copy number, transcriptional and protein level with patients’ survival and drug response. Copy number analysis revealed a predominant pattern of gains occurring in S100 genes clustering in the 1q21 locus. In general, gains of genes encoding S100 family members associated with worse patient survival. However, S100 gene copy number and S100 gene expression did not necessarily correlate, and high expression of S100A4 associated with poor patient survival. Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat. Combined proteomic and pharmacological data exhibited significant negative association of S100 members (S100A4, S100A8, and S100A9) with proteasome inhibitors and panobinostat. Clinically, the higher expression of S100A4 and S100A10 were significantly linked to shorter progression free survival in patients receiving carfilzomib-based therapy. The results indicate an association and highlight the potential functional importance of S100 members on chromosome 1q21 in the development of MM and resistance to established myeloma drugs, including proteasome inhibitors.

scholarly journals Renal Endothelin-1 and Endothelin Receptor Type B Expression in Glomerular Diseases with Proteinuria

2001 ◽  
Vol 12 (11) ◽  
pp. 2321-2329
Author(s):  
INGO LEHRKE ◽  
RÜDIGER WALDHERR ◽  
EBERHARD RITZ ◽  
JÜRGEN WAGNER
Keyword(s):  
Gene Expression ◽  
Renal Disease ◽  
Protein Expression ◽  
Mrna Expression ◽  
Iga Nephropathy ◽  
Receptor Type ◽  
Lower Grade ◽  
Glomerular Diseases ◽  
Control Subjects ◽  
Immunohistochemical Analyses

Abstract. The endothelin (ET) system has been studied extensively in experimental models of progressive chronic renal disease, but there is limited information regarding the ET system in renal patients. First, the expression of human ET-1, as well as ET receptor type A (ET-RA) and ET-RB, was studied in 26 renal biopsies from patients with different renal diseases. Gene expression was assessed by quantitative reverse transcription-PCR. Second, ET-1 and ET-RBprotein expression and localization were examined, by immunohistochemical analyses, among a homogeneous cohort of 16 patients with IgA nephropathy and different degrees of proteinuria. ET-RBmRNA expression was threefold higher among patients with higher-grade proteinuria [≥2 g/24 h,n= 10; OD ratio (ODR),i.e., wild-type/mutant mRNA ratio, 1.81 ± 0.3], compared with patients with lower-grade proteinuria (<2 g/24 h,n= 8; ODR, 0.63 ± 0.1;P< 0.01) or control subjects (n= 9; ODR, 0.57 ± 0.1;P< 0.01). ET-1 gene expression was significantly higher among patients with higher-grade proteinuria, compared with patients with lower-grade proteinuria (P< 0.01) or control subjects (P< 0.05). ET-RAmRNA expression was not different among the groups. Patients with higher-grade proteinuria who were receiving angiotensin-converting enzyme inhibitors exhibited significantly (P< 0.05) lower ET-1 and ET-RBmRNA expression, which was comparable to that of control subjects. By using immunohistochemical analyses, an association between proteinuria and expression of ET-1 and ET-RBin proximal tubular epithelial cells and of ET-1 in glomeruli was confirmed in the separate cohort of patients with IgA nephropathy. It is concluded that the increased ET-RBand ET-1 mRNA and protein expression observed in animal models of renal disease is also demonstrable among patients with renal disease and high-grade proteinuria.

Perforin gene expression in T lymphocytes correlates with disease activity in immunoglobulin A nephropathy

1992 ◽  
Vol 82 (4) ◽  
pp. 461-468 ◽  
Author(s):  
Tsukasa Nakamura ◽  
Isao Ebihara ◽  
Shiori Osada ◽  
Ko Okumura ◽  
Yasuhiko Tomino ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Lymphocytes ◽  
Disease Activity ◽  
Mrna Expression ◽  
Iga Nephropathy ◽  
Matched Control ◽  
Immunoglobulin A ◽  
Renal Tissue ◽  
Control Subjects ◽  
Protein Excretion

1. We studied perforin gene expression in T lymphocytes obtained from 26 patients with IgA nephropathy and from 15 healthy age-matched control subjects. 2. The majority of patients with IgA nephropathy (96%) had elevated perforin mRNA expression, whereas no perforin mRNA expression was detected in the T lymphocytes of normal control subjects. 3. A positive correlation was noted between perforin mRNA expression and urinary protein excretion. 4. Perforin mRNA expression correlated also with the histopathology in the renal tissue of patients with IgA nephropathy. 5. Sixty per cent of patients with grade III or IV histopathology had high perforin mRNA expression in T lymphocytes [more than (++)]. 6. These studies suggest that disregulation of perforin gene expression in T lymphocytes may be associated with the progression of IgA nephropathy and could be used as an indicator of disease activity.

Mechanisms of Bcl-2 Protein Expression in Diffuse Large B-Cell Lymphoma (DLBCL).

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 26-26
Author(s):  
Pedro Farinha ◽  
Gwyn Bebb ◽  
Reiner Siebert ◽  
Doug Horsman ◽  
Joseph M. Connors ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Expression Profiling ◽  
Copy Number ◽  
Gene Copy Number ◽  
Copy Number Gain ◽  
Gene Copy ◽  
Cell Of Origin ◽  
Bcl2 Protein ◽  
Bcl2 Gene

Abstract Background: Bcl-2 protein expression is an important biomarker in DLBCL. Gene expression profiling also has prognostic relevance in DLBCL, establishing cell-of-origin (GCB vs non-GCB) as an important predictor of survival. Using tissue microarrays (TMA), immunohistochemical staining can be used to provide biomarker data that correlates closely with the results of gene expression profiling in predicting outcome (Hans et al, Blood 103; 275–82: 2004). The t(14;18) can be detected in DLBCL, with frequencies varying between 5–40%. The aim of this study was to clarify the different mechanisms leading to Bcl-2 expression in a cohort of patients with DLBCL. Methods: The study group consisted of 94 patients with de novo DLBCL, all with a clonal karyotype at diagnosis and treated with curative intent. A TMA was constructed with duplicate 0.6mm cores and stained for Bcl-2, CD10, Bcl-6, MUM1 and FOXP1. Cases were called positive if more than 30% of the tumor cells expressed a given protein. Cases were defined as GCB if they were CD10+. Non-GCB was defined as CD10−, MUM1+ and/or FOXP1+. Cytogenetic studies were performed routinely and locus-specific FISH was performed using commercially available Vysis probes (dual-color LSI IGH/BCL2) to detect the t(14;18). Unbalanced increases in BCL2 gene copy number were determined by comparison of BCL2 and IGH signals and correlation with the karyotype. Results: The IPI was highly predictive of overall survival (OS) (p &lt; 0.00001). The t(14;18) was detected by both routine cytogenetics and FISH in 24 (25%) cases, but did not predict survival (p = 0.78). None of the non-GCB cases harbored a t(14;18). The t(14;18) and isolated BCL2 copy number gain were mutually exclusive. Expression of Bcl-2 protein and GCB-type immunostaining profile each predicted OS (p = 0.008 and 0.03, respectively). Expression of Bcl-2 was imperfectly correlated with either the t(14;18) or a non-GCB immunostaining profile, but was highly correlated with cases harboring an increased gene copy number for BCL2 (see Table, χ2 p=0.005). Increased BCL2 gene copy number did not predict OS (p = 0.43), a not unexpected finding as it accounts for only a proportion of Bcl-2 protein-positive cases. Cases lacking both the t(14;18) and increased BCL2 copy number were deemed cytogenetically “normal”, accounting for 47 cases. These were distributed between the GCB (42%) and non-GCB cases (62%). Of the cytogenetically “normal” cases, 35% of the GCB and 63% of the non-GCB expressed Bcl-2 protein. BCL2 Probe Result GCB(55) Non-GCB(39) n Bcl2 protein + n Bcl2 protein + t(14;18)(q32;21) 24 18 0 0 ⇑ Gene Copy# 8 6 15 14 “Normal” 23 8 24 15 Conclusions: We conclude that multiple mechanisms are responsible for Bcl-2 expression in DLBCL. Non-GCB cases do not harbor the t(14;18), more commonly have isolated BCL2 gene copy number gain and have a higher percentage of cytogenetically “normal” BCL2 protein-positive cases. The latter finding suggests a prominent role for transcriptional up-regulation of the BCL2 gene resulting from constitutive activation of NF- κB. DLBCL cases with a t(14;18) are always GCB and never show isolated BCL2 gene copy number gains, suggesting that these two events are mutually exclusive. The impact of other mechanisms (e.g. epigenetic changes, promoter hypomethylation) deregulating BCL2 expression requires further study. Bcl-2 protein expression and cell-of-origin (GCB vs non-GCB) are predictive biomarkers in DLBCL.

HER2 activity in solid tumors.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23121-e23121
Author(s):  
Lara Ann Kujtan ◽  
Scott Morris ◽  
Janakiraman Subramanian
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Solid Tumors ◽  
Copy Number ◽  
Significant Proportion ◽  
Copy Number Gain ◽  
Tumor Type ◽  
Breast Cancers ◽  
Distinctive Pattern ◽  
Tumor Types

e23121 Background: ERBB2 is a member of the human epidermal growth factor receptor family. HER2 expression that is immunohistochemistry (IHC) 3+ or IHC 2+ with copy number gain is an effective predictor for treatment with trastuzumab in breast and gastroesophageal cancers. Here we present an analysis on HER2 activity measured by IHC, mRNA expression and copy number variation (CNV) across a variety of solid tumors. Methods: The study population consists of patients diagnosed with solid tumors (n = 856) that underwent a Paradigm Diagnostic Cancer Test during 2016. We then analyzed tumor types that tested positive for HER2 by IHC (3+), CNV and/or mRNA expression. Results: We identified 365 (43%) patients positive for HER2 by IHC, 258 (30%) had high HER2mRNA expression and 41 (5%) had amplification by CNV. Seventy-five patients were HER2 IHC 3+ or 2+/CNV positive. The proportion of HER2 IHC 3+ or 2+/CNV positive tumors in each tumor type was as follows: breast cancer 41 (18.5%), NSCLC 10 (8.1%), colorectal 6 (6.7%), esophago-gastric 3 (10%,) urothelial/bladder 3 (16%), biliary 2 (28.6%), ovarian cancer 2 (5.1%) and pancreas 1 (3.1%). Using copy number gain as the gold standard, across all tumor types, an IHC of 3+ had a 90.2% sensitivity and a 95.6% specificity. In the same analysis with breast cancers omitted, the sensitivity was 75%, and specificity 96.8%. Whereas high mRNA expression had a sensitivity of 97.6% and specificity of 73.3%, omitting breast cancers, the sensitivity was 93.8% and specificity 73.2%. Conclusions: HER2 activity was identified in a wide variety of solid tumors and a small but significant proportion of these tumors maybe candidates for treatment with HER2 inhibitors such as trastuzumab. Our analysis also identified that HER2 activity in breast cancers has a distinctive pattern which was not seen in other tumor types. HER2 IHC 3+ expression was much less sensitive among other tumor types compared to breast cancer. mRNA expression, while remaining sensitive among other tumor types, is not specific, even among breast cancer patients. Our analysis also identified that HER2 activity in breast cancers has a distinctive pattern which was not seen in other tumor types.

scholarly journals Impaired Insulin-Stimulated Expression of the Glycogen Synthase Gene in Skeletal Muscle of Type 2 Diabetic Patients Is Acquired Rather Than Inherited1

2000 ◽  
Vol 85 (4) ◽  
pp. 1584-1590 ◽  
Author(s):  
Xudong Huang ◽  
Allan Vaag ◽  
Mona Hansson ◽  
Jianping Weng ◽  
Esa Laurila ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Mrna Expression ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Diabetic Patients ◽  
Mrna Levels ◽  
Control Subjects ◽  
Chronic Hyperglycemia

To examine whether defective muscle glycogen synthase (GYS1) expression is associated with impaired glycogen synthesis in type 2 diabetes and whether the defect is inherited or acquired, we measured GYS1 gene expression and enzyme activity in muscle biopsies taken before and after an insulin clamp in 12 monozygotic twin pairs discordant for type 2 diabetes and in 12 matched control subjects. The effect of insulin on GYS1 fractional activity, when expressed as the increment over the basal values, was significantly impaired in diabetic (15.7 ± 3.3%; P &lt; 0.01), but not in nondiabetic (23.7 ± 1.8%; P = NS) twins compared with that in control subjects (28.1 ± 2.3%). Insulin increased GYS1 messenger ribonucleic acid (mRNA) expression in control subjects (from 0.14 ± 0.02 to 1.74 ± 0.10 relative units; P &lt; 0.01) and in nondiabetic (from 0.24 ± 0.05 to 1.81 ± 0.16 relative units; P &lt; 0.01) and diabetic (from 0.20 ± 0.07 to 1.08 ± 0.14 relative units; P &lt; 0.01) twins. The effect of insulin on GYS1 expression was, however, significantly reduced in the diabetic (P &lt; 0.003), but not in the nondiabetic, twins compared with that in control subjects. The postclamp GYS1 mRNA levels correlated strongly with the hemoglobin A1c levels (r = −0.61; P &lt; 0.001). Despite the decrease in postclamp GYS1 mRNA levels, the GYS1 protein levels were not decreased in the diabetic twins compared with those in the control subjects (2.10 ± 0.46 vs. 2.10 ± 0.34 relative units; P = NS). We conclude that 1) insulin stimulates GYS1 mRNA expression; and 2) impaired stimulation of GYS1 gene expression by insulin in patients with type 2 diabetes is acquired and most likely is secondary to chronic hyperglycemia.

Osmoregulation and gene expression of Na+/K+ ATPase in families of Atlantic salmon (Salmo salar) smolts

2005 ◽  
Vol 62 (11) ◽  
pp. 2661-2672 ◽  
Author(s):  
P Mackie ◽  
P A Wright ◽  
B D Glebe ◽  
J S Ballantyne
Keyword(s):  
Gene Expression ◽  
Atlantic Salmon ◽  
Atpase Activity ◽  
Mrna Expression ◽  
Salmo Salar ◽  
Plasma Osmolality ◽  
Atlantic Salmon Salmo Salar ◽  
Significant Difference ◽  
The Family ◽  
Osmoregulatory Ability

This study reports that families of Atlantic salmon (Salmo salar) smolts vary in their ability to osmo- and iono-regulate following abrupt transfer to cold seawater. Eleven families of Atlantic salmon 0+ smolts were held in fresh water (2.4–4 °C) or transferred to seawater (1.9–4 °C) and sampled 0 h, 24 h, 96 h, and 30 days post-transfer. Plasma osmolality was significantly different among the families after 24 h of seawater exposure. The family with the lowest osmolality at 24 h also displayed the lowest plasma Cl– concentrations as well as the highest gill Na+/K+ ATPase activity. Gill mRNA expression of the Na+/K+ ATPase α1b isoform increased following seawater exposure, whereas the α1a isoform decreased, but there was no significant difference among families. Taken together, the interfamily differences in osmoregulatory ability are correlated with gill Na+/K+ ATPase activity but not the expression of two salinity-sensitive Na+/K+ ATPase isoforms. Furthermore, the data indicate that family differences in gill Na+/K+ ATPase activity were only apparent when assayed at the sampling temperature (4 °C) and not at a higher assay temperature (10 °C).

Sign in / Sign up

Export Citation Format

Share Document