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At least 649 records · Page 36Linked to original sources
PubMed2004

[Mutation of Indy(p115) increases the life expectancy of imago of Drosophila melanogaster depending on sex and genetic background].

The Indyp115 allele in heterozygous state almost doubles the life span of adult Drosophila melanogaster, and this effect largely depends on the strain used for obtaining heterozygotes. Male and female life span depends on Indyp115 to a different degree. Apart from Indyp115 heterozygotes, sexual dimorphism for life span was also observed in strain Hikone-AW, but not in OregonR and TM3 balancer. In heterozygotes Indyp115/OR, both the average life span and female reproductive period increased as compared to OR control. No substantial increase in female reproductive period in Indyp115/Hk heterozygotes was found. In homozygotes for allele Indyp115, we have previously revealed two phases of embryotic lethality and lethality at the larval and pupa stages. Thus, allele Indyp115 has a double and opposite effect on Drosophila viability. On the one hand, it extends the life span of adult flies, on the other, decreases survival at preimaginal stages.

Alleles↗
PubMed2005

ASD--lessons on genetic background from transgenic mice with inactive gene encoding metalloprotease, Tolloid-like 1 (TLL1).

Congenital heart defects still constitute serious medical problems. The background of such defects, however, is poorly understood. Little is also known about their pattern of inheritance. Lack of atrial and ventricular septum closures counts for a significant percentage of all congenital heart defects. Individuals harboring such defects always suffer poor quality of life. The only way to help those patients is cardiac surgery. Several genes have been implicated in the process of controlling heart development. Recent studies on transgenic mice null for tolloid-like 1 (tll1) gene revealed factors possibly involved in signaling pathways that, when absent, might affect heart development and cause problems mimicking those observed in atrial septal defects (ASDs). Lack of activity of this metalloprotease caused incomplete closure of the septum in murine fetal hearts and led to death in mid-gestation due to severe circulation problems. tll1 gene is located on the long arm of chromosome 4 (4q32-q33). The gene comprises of 6654 nucleotides and it encodes a protein 1013 amino acids long. Its human homologue tll1 is poorly investigated and until now no particular disorders have been linked to mutations in this gene.

Animals↗
PubMed2006

Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background.

Aggressive fibromatosis, usually called desmoid tumor develops from muscle connective tissue, fasciae and aponeuroses. This neoplasm is composed of spindle (fibrocyte-like) cells. As regards the site, aggressive fibromatoses can be divided into: extra-abdominal in the area of the shoulder and pelvic girdle or chest and neck wall; abdominal in abdominal wall muscles; intra-abdominal concerning pelvis, mesentery connective tissue or retroperitoneal space. Desmoid tumor is a neoplasm which rarely turns malignant and is non-metastasizing but demonstrates ability to local infiltration into tissue and is characterized by high risk of recurrence (25-65%) after surgical treatment. Desmoid tumor etiology is uncertain. This neoplasm occurs in sporadic (idiopathic) form and is also associated with some familial neoplastic syndromes. Most sporadic cases of aggressive fibromatosis contain a somatic mutation in either the adenomatous polyposis coli (APC) or beta-catenin genes. Sporadic tumors are more frequent in women than in men from 2 : 1 to 5 : 1. In about 10-15 per cent of patients with familial adenomatous polyposis (FAP), aggressive fibromatosis is a parenteral manifestation of this familial syndrome conditioned by APC gene mutation. Abdomen injury--most frequently due to surgery is said to play an important role in the initiation of fibrous tissue proliferative process in the cases of abdominal and intra abdominal forms. High cells growth potential with relatively high local malignancy is observed in about 10% of cases with sporadic tumors as well as in those FAP-associated.

Desmoid Tumors↗
PubMed2006

Enhanced expression of Ca2+ channel alpha1A and beta4 subunits and phosphorylated tyrosine hydroxylase in the adrenal gland of N-type Ca2+ channel alpha1B subunit-deficient mice with a CBA/JN genetic background.

Electrophysiologic studies have demonstrated that adrenal medulla chromaffin cells express voltage-dependent P/Q-, N-, L-, and R-type Ca2+ channels and that these channels regulate release of norepinephrine and epinephrine. However, N-type Ca2+ channel alpha1B-deficient mice with a CBA/JN background show normal plasma norepinephrine and epinephrine levels, presumably owing to compensation by other gene(s). To examine the expression patterns of the P/Q-type alpha1A, L-type alpha1C/alpha1D, and R-type alpha1E, beta1, beta2, beta3, and beta4 subunits, as well as of tyrosine hydroxylase (Th), dopamine beta hydroxylase (Dbh), and phenylethanolamine-N-methyltransferase (Pnmt) in the adrenal gland of alpha1B-deficient mice, we used real-time quantitative reverse transcription-polymerase chain reaction and Western blot analyses. The expression levels of alpha1A, beta4, Th, and Th phosphorylated at serine 40 were higher in homozygous mice than in wild-type and heterozygous mice, but the expression levels of alpha1C, alpha1D, alpha1E, beta1, beta2, beta3, Dbh, and Pnmt did not differ among wild-type, heterozygous, and homozygous mice. These results suggest that the compensatory mechanisms to maintain normal levels of epinephrine and norepinephrine in the adrenal gland of N-type Ca2+ channel alpha1B-deficient mice include increased expression of alpha1A and beta4 subunits and increased catecholamine biosynthetic activity.

Adrenal Glands↗
PubMed1991

The effect of the genetic background on the development and function of accumulating YE1/19.1+ cells in lpr mice.

It has been demonstrated that the single autosomal recessive lpr gene is capable of inducing autoimmunity in various strains of mice. Moreover, it is generally accepted that this is an indirect effect of the accumulation of an unusual T lymphocyte subset. Although a thymus is essential for the initiation of the lymphadenopathy, adult thymectomy cannot delay the development of the disease. In this study we report that the degree of lymphadenopathy can be assessed utilizing the YE1/19.1 monoclonal antibody. This antibody recognizes a surface antigen found on the EL 4 tumor lines and all "double negative" nonresponsive T cells from lpr gene expressing mice. We then constructed radiation-induced chimeras to determine whether a normal thymic and extrathymic milieu had any effect on the development and function of the YE1/19.1+ T cells responsible for the lymphadenopathy. It was found that the spleens of B6-lpr----B6-lpr chimeras demonstrated a marked accumulation of the YE1/19.1 positive cells. However, the spleens of B6-lpr----B6 chimeras were shown to contain very few YE1/19.1 positive cells. These differences were also reflected in the amount of anti-DNA antibodies produced by each of the chimeras, the B6 recipients producing very little autoantibody. Once isolated by panning it was found that the cells from either chimera failed to respond to mitogenic signals. Our findings support the possibility that the lpr gene can function in the thymus and/or the periphery of the animal to limit the numbers of accumulating T cells.

Animals↗