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At least 91 records · Page 5Linked to original sources
PubMed2000

MinK subdomains that mediate modulation of and association with KvLQT1.

KvLQT1 is a voltage-gated potassium channel expressed in cardiac cells that is critical for myocardial repolarization. When expressed alone in heterologous expression systems, KvLQT1 channels exhibit a rapidly activating potassium current that slowly deactivates. MinK, a 129 amino acid protein containing one transmembrane-spanning domain modulates KvLQT1, greatly slowing activation, increasing current amplitude, and removing inactivation. Using deletion and chimeric analysis, we have examined the structural determinants of MinK effects on gating modulation and subunit association. Coexpression of KvLQT1 with a MinK COOH-terminus deletion mutant (MinK DeltaCterm) in Xenopus oocytes resulted in a rapidly activated potassium current closely resembling currents recorded from oocytes expressing KvLQT1 alone, indicating that this region is necessary for modulation. To determine whether MinK DeltaCterm was associated with KvLQT1, a functional tag (G55C) that confers susceptibility to partial block by external cadmium was engineered into the transmembrane domain of MinK DeltaCterm. Currents derived from coexpression of KvLQT1 with MinK DeltaCterm were cadmium sensitive, suggesting that MinK DeltaCterm does associate with KvLQT1, but does not modulate gating. To determine which MinK regions are sufficient for KvLQT1 association and modulation, chimeras were generated between MinK and the Na(+) channel beta1 subunit. Chimeras between MinK and beta1 could only modulate KvLQT1 if they contained both the MinK transmembrane domain and COOH terminus, suggesting that the MinK COOH terminus alone is not sufficient for KvLQT1 modulation, and requires an additional, possibly associative interaction between the MinK transmembrane domain and KvLQT1. To identify the MinK subdomains necessary for gating modulation, deletion mutants were designed and coexpressed with KvLQT1. A MinK construct with amino acid residues 94-129 deleted retained the ability to modulate KvLQT1 gating, identifying the COOH-terminal region critical for gating modulation. Finally, MinK/MiRP1 (MinK related protein-1) chimeras were generated to investigate the difference between these two closely related subunits in their ability to modulate KvLQT1. The results from this analysis indicate that MiRP1 cannot modulate KvLQT1 due to differences within the transmembrane domain. Our results allow us to identify the MinK subdomains that mediate KvLQT1 association and modulation.

Animals↗
PubMed2004

An LQT mutant minK alters KvLQT1 trafficking.

Cardiac I(Ks), the slowly activated delayed-rectifier K(+) current, is produced by the protein complex composed of alpha- and beta-subunits: KvLQT1 and minK. Mutations of genes encoding KvLQT1 and minK are responsible for the hereditary long QT syndrome (loci LQT1 and LQT5, respectively). MinK-L51H fails to traffic to the cell surface, thereby failing to produce effective I(Ks). We examined the effects that minK-L51H and an endoplasmic reticulum (ER)-targeted minK (minK-ER) exerted over the electrophysiology and biosynthesis of coexpressed KvLQT1. Both minK-L51H and minK-ER were sequestered primarily in the ER as confirmed by lack of plasma membrane expression. Glycosylation and immunofluorescence patterns of minK-L51H were qualitatively different for minK-ER, suggesting differences in trafficking. Cotransfection with the minK mutants resulted in reduced surface expression of KvLQT1 as assayed by whole cell voltage clamp and immunofluorescence. MinK-L51H reduced current amplitude by 91% compared with wild-type (WT) minK/KvLQT1, and the residual current was identical to KvLQT1 without minK. The phenotype of minK-L51H on I(Ks) was not dominant because coexpressed WT minK rescued the current and surface expression. Collectively, our data suggest that ER quality control prevents minK-L51H/KvLQT1 complexes from trafficking to the plasma membrane, resulting in decreased I(Ks). This is the first demonstration that a minK LQT mutation is capable of conferring trafficking defects onto its associated alpha-subunit.

Animals↗
PubMed2005

Final amended report on the safety assessment of Mink Oil.

Mink Oil, obtained from the fatty tissues of minks, is a mixture of the natural glycerides of 14 to 20 carbon chain fatty acids. There are 100 current reported uses as a hair-conditioning agent, an occlusive skin-conditioning agent, and as a surfactant; up to a maximum concentration of 3%. Mink Oil is manufactured by harvesting animal hides and scraping the fat layer from the hide. It is rendered and refined using high temperature processes (230 degrees F to 240 degrees F) and saponification to reduce free fatty acids. Analyses demonstrate that Mink Oil can be substantially free of impurities, including pesticides. Mink Oil does not absorb significant UVA or UVB radiation. In a clinical test of skin penetration, 1 h after application, Mink Oil was detected on the skin surface of all five panelists; it was detected within the stratum corneum in 2/5 panelists. Mink Oil has an oral LD50 of > 64.0 cc/kg in albino rats. No erythema or edema was noted after refined Mink Oil was applied for 24 h to intact and scarified area of albino rabbits. A 50% dilution of a Mink Oil cream did not sensitize guinea pigs in a maximization test. Mink Oil was not an ocular irritant to albino rabbits. Clinical studies using single occlusive patches found no irritation with up to 2.8% Mink Oil, although transient mild to no irritation was noted in two exaggerated-use studies. Mink Oil is used in aerosols and sprays. Although there are no inhalation toxicity data available on Mink Oil, the available data on particle sizes of cosmetic aerosols and sprays indicates diameters more than an order of magnitude larger than the diameter of respirable particles. Most of the glycerides in Mink Oil are triglycerides (glyceryl triesters), the safety of which has been substantiated in previous safety assessments; e.g., dermal absorption is nil to slight; there is little or no acute, subchronic, or chronic oral toxicity; dermal application was not associated with significant irritation or sensitization; ocular exposures were, at most, mildly irritating; most of the genotoxicity test systems are negative; use as vehicles in carcinogenicity testing of other chemicals has produced no adverse reaction; and clinical tests produce no irritation or sensitization reactions--but, they may enhance the of penetration of other chemicals. Formulators should be aware of the possible penetration-enhancing properties of Mink Oil. Although pesticide residues have been analyzed and found to be below levels of detection, the Panel is concerned that the available data suggesting the absence of pesticide residues in Mink Oil are limited. The Panel advised the industry that the total polychlorinated biphenyl (PCB)/pesticide contamination should be limited to not more than 40 ppm, with not more than 10 ppm for any specific residue.

Adipose Tissue↗
PubMed1996

Melatonin-induced downregulation of uterine prolactin receptors in mink (Mustela vison).

A study was conducted to investigate the effects of exogenous melatonin on serum concentrations of estradiol-17 beta (E2) and progesterone (P4) and uterine prolactin (PRL) receptor concentrations in mated mink. In Experiment 1, two groups of adult, standard dark, female mink were mated to fertile males on March 8 or 9. On March 16, mink in group 1 (N = 8) received an empty Silastic implant inserted sc in the interscapular region and served as controls. Mink in group 2 (N = 8) received an implant containing 10 mg crystalline melatonin. On April 2, all animals were lightly anesthetized and blood samples collected via cardiac puncture were analyzed for serum concentrations of E2 and P4. Animals were subsequently sacrificed and uterine samples collected for analysis of PRL receptor concentrations. In Experiment 2, adult female mink were assigned randomly to three treatment groups and mated to fertile males between March 6 and 9. On March 16, mink in group 1 (N = 6) received empty Silastic implants and served as controls. Mink in group 2 (N = 6) received a Silastic implant containing 10 mg melatonin. Animals in group 3 (N = 6) received an implant containing 10 mg melatonin and in addition each mink was given daily sc injections of P4 (1 mg) from March 21 to April 5. At this time the mink were sacrificed, the number of implantation sites recorded, and uteri collected for quantification of PRL receptors. In Experiment 1, exogenous melatonin reduced serum P4 concentrations to almost nondetectable levels (controls, 8.08 +/- 0.73 vs treated, 0.82 +/- 0. 12 ng/ml; P < 0.001) and resulted in increased concentrations of E2 (controls, 13.3 +/- 1.9 vs treated, 22.0 +/- 1.9 pg/ml; P < 0.01). Uterine PRL receptor concentrations decreased (P < 0.05) from 37.74 +/- 9.37 fmol/mg protein (controls) to 23.74 +/- 9.03 fmol/mg protein in response to melatonin treatment. In those mink treated with melatonin plus P4 (Experiment 2), uterine PRL receptor concentrations were increased to levels not significantly different than those of controls. None of the mink treated with melatonin alone or in combination with P4 exhibited implantation. Uteri of mink treated with melatonin or melatonin plus P4 did not differ in weight but tended to weigh less than uteri of control mink. These data suggest that a high systemic ratio of P4 to E2 is essential for production of the uterine PRL receptor in mink and supports the findings of others that implantation in mink cannot be initiated with P4 alone.

Animals↗
PubMed1991

Mink-mouse interspecific hybridomas.

Mink-mouse interspecific hybridomas were produced by fusion of the american mink spleen cells with the NSO cells. Seven cloned lines of the mink-mouse hybridoma were isolated, and their functional mink Ig secretion and karyological characteristics are given. During cytogenetic analysis of mink-mouse hybridoma cell lines, we observed the elimination of mink chromosomes, and inter- and intralineral variability of the numbers of the cells with particular quantities of mink DNA. We did not find that the characteristic peculiarities of mink DNA distribution in the hybridoma cell lines had any bearing upon the secretion or non-secretion of mink Ig. There was no synthesis of lambda-L-chains of mink Ig in line 7 cells because the line lost the lambda-gene. With the aid of in situ hybridization with 3H-labeled total mink DNA, a considerable transformation of hybridoma cell karyotype was observed. Multiple integration of the mink DNA into mouse chromosomes and the appearance of chromosomes not characteristic for either the mink or mouse parent cells were noted. Increasing numbers of cells with translocations of mink chromosomes fragments into mouse chromosomes were found in the hybridoma lines cultivated for lengthy periods.

Animals↗
PubMed1984

Cotransfer and phenotypic stabilisation of syntenic and asyntenic mink genes into mouse cells by chromosome-mediated gene transfer.

By means of metaphase chromosomes, the genes for mink thymidine kinase (TK) and hypoxanthine-phosphoribosyltransferase (HPRT) were transferred to mutant mouse cells, LMTK-, A9 (HPRT-) and teratocarcinoma cells, PCC4-aza 1 (HPRT-). Eighteen colonies were isolated from LMTK- (series A), 9 from A9 (series B) and none from PCC4-aza 1. The transformed clones contained mink TK or HPRT. Analysis of syntenic markers in series B demonstrated that one clone contained mink glucose-6-phosphate dehydrogenase (G6PD) and the other alpha-galactosidase; in series A, nine clones contained mink galactokinase (GALK) and six mink aldolase C (ALDC). Analysis of 12 asyntenic markers located in ten mink chromosomes showed the presence of only aconitase-1 (ACON1) (the marker of mink chromosome 12) in three clones of series A. The clones lost mink ACON1 between the fifth to tenth passages. Cytogenetic analysis established the presence of a fragment of mink chromosome 8 in eight clones of series A, but not in series B. The clones of series A lost mink TK together with mink GALK and ALDC during back-selection; in B, back-selection retained mink G6PD. No stable TK+ phenotype was detected in clones with a visible fragment of mink chromosome 8. Stability analysis demonstrated that about half of the clones of series B have stable HPRT+ phenotype whereas only three clones of series A have stable TK+ phenotype. It is suggested that the recipient cells, LMTK- and A9, differ in their competence for genetic transformation and integration of foreign genes.

Animals↗
PubMed2003

The effects of diisopropylmethylphosphonate, a by-product of the production of sarin and a contaminant in drinking water at the Rocky Mountain Arsenal, on female mink.

This paper challenges the interpretation of the report on the effects of DIMP on mink with respect to mortality causation and organ-specific toxicity (i.e., liver, kidney, and thymus). During the second generation (F(1)) of a two generation toxicity study by on the effects of DIMP on female brown Ranch Wild mink, a cluster of six premature deaths occurred, being attributed to an unintentional anesthetic overdose that induced a stress-related syndrome rather than DIMP exposure. The present paper reveals that the six adult female mink (i.e., four DIMP treated and two controls) had medical conditions that pre-existed the administration of anesthetic. Three of the four DIMP-exposed mink that died displayed evidence of medically significant red blood cell damage and immune system involvement, while all six mink had elevated blood serum enzymes (ALT/AST) indicative of liver damage along with confirmatory histopathology indicating severe liver damage. These findings challenge the conclusion of Bucci et al. that the six mink deaths were solely caused by stress induced by anesthesia, and suggest DIMP related pre-existing conditions (e.g., red blood cell damage and elevated ALT/AST) may have contributed to the deaths in DIMP-treated mink. also inexplicably combined both the pregnant and non-pregnant animal data, thereby precluding an assessment of the effects of DIMP on pregnant and non-pregnant mink. A re-evaluation of the findings of the data revealed that pregnancy/lactation significantly influenced the incidence of physiologic alterations and histological lesions in the female mink for the kidney, liver, and thymus, findings that were masked by the combining of pregnant and non-pregnant results. Further evaluations indicated that DIMP treatment also significantly induced liver lesions in pregnant mink and kidney lesions in both pregnant and non-pregnant mink. These findings challenge the conclusions of Bucci et al. concerning the effects of DIMP on mink as well as identify for the first time that pregnancy/lactation in mink is a risk factor in the induction of thymic atrophy and the elevation of serum ALT/AST.

Animals↗
PubMed1996

Investigation of an outbreak of Aleutian disease on a commercial mink ranch.

OBJECTIVE: To determine the modes of transmission of Aleutian mink disease in a natural outbreak. ANIMALS: 5,580 black and 9,087 brown mink from a ranch with an outbreak of Aleutian mink disease. PROCEDURE: Each mink had serum tested by counter-electrophoresis for Aleutian disease antibody. If a mink was seropositive for Aleutian disease virus by counter-electrophoresis, it was considered to be infected. Correlation of prevalence of the disease in kits and parents was determined. Spatial arrangement of infected and un-infected mink also was studied. RESULTS: Infected black dams were more likely to produce infected kits than were uninfected dams. In contrast, infected black sires were less likely to produce infected kits than were uninfected sires. In brown mink, in which prevalence of Aleutian disease was lower, transmission from infected dams and sires to kits was apparent. Infected black mink appeared to be more efficient in transmitting the disease horizontally than were infected brown mink. Although the spatial arrangement of infected mink indicated that mechanical transmission of the disease may be the most efficient mode of horizontal transmission, airborne transmission also occurred. CONCLUSIONS AND CLINICAL RELEVANCE: Infected sires with nonprogressive Aleutian disease may confer protection to their kits in the face of a severe outbreak. Brown mink may be less able to transmit the virus horizontally than are black mink. Airborne transmission is substantial, but may not be as efficient as mechanical transmission.

Aleutian Mink Disease↗