scholarly journals Developmental Expression of Wild-Type and Mutant Presenilin-1 in Hippocampal Neurons from Transgenic Mice: Evidence for Novel Species-Specific Properties of Human Presenilin-1

1999 ◽  
Vol 5 (8) ◽  
pp. 542-554 ◽  
Author(s):  
Lyne Lévesque ◽  
Willem Annaert ◽  
Katleen Craessaerts ◽  
Paul M. Mathews ◽  
Mary Seeger ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Hippocampal Neurons ◽  
Novel Species ◽  
Developmental Expression ◽  
Presenilin 1 ◽  
Wild Type ◽  
Species Specific

Transcriptome Differences Between the Frontal Cortex and Hippocampus of Wild-Type and Humanized Presenilin-1 Transgenic Mice

2005 ◽  
Vol 13 (12) ◽  
pp. 1041-1051 ◽  
Author(s):  
Travis Unger ◽  
Zeljka Korade ◽  
Orly Lazarov ◽  
David Terrano ◽  
Nina F. Schor ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Frontal Cortex ◽  
Presenilin 1 ◽  
Wild Type

scholarly journals Presenilin 1 mediates the turnover of telencephalin in hippocampal neurons via an autophagic degradative pathway

2004 ◽  
Vol 166 (7) ◽  
pp. 1041-1054 ◽  
Author(s):  
Cary Esselens ◽  
Viola Oorschot ◽  
Veerle Baert ◽  
Tim Raemaekers ◽  
Kurt Spittaels ◽  
...  
Keyword(s):  
Half Life ◽  
Cathepsin D ◽  
Hippocampal Neurons ◽  
Transmembrane Domain ◽  
Presenilin 1 ◽  
Wild Type ◽  
Degradative Pathway ◽  
Autophagic Vacuoles ◽  
Secretase Activity ◽  
Lysosomal Proteins

Presenilin 1 (PS1) interacts with telencephalin (TLN) and the amyloid precursor protein via their transmembrane domain (Annaert, W.G., C. Esselens, V. Baert, C. Boeve, G. Snellings, P. Cupers, K. Craessaerts, and B. De Strooper. 2001. Neuron. 32:579–589). Here, we demonstrate that TLN is not a substrate for γ-secretase cleavage, but displays a prolonged half-life in PS1−/− hippocampal neurons. TLN accumulates in intracellular structures bearing characteristics of autophagic vacuoles including the presence of Apg12p and LC3. Importantly, the TLN accumulations are suppressed by adenoviral expression of wild-type, FAD-linked and D257A mutant PS1, indicating that this phenotype is independent from γ-secretase activity. Cathepsin D deficiency also results in the localization of TLN to autophagic vacuoles. TLN mediates the uptake of microbeads concomitant with actin and PIP2 recruitment, indicating a phagocytic origin of TLN accumulations. Absence of endosomal/lysosomal proteins suggests that the TLN-positive vacuoles fail to fuse with endosomes/lysosomes, preventing their acidification and further degradation. Collectively, PS1 deficiency affects in a γ-secretase–independent fashion the turnover of TLN through autophagic vacuoles, most likely by an impaired capability to fuse with lysosomes.

Altered IP3-dependent intracellular Ca2+ pools of hippocampal neurons in presenilin-1 mutant transgenic mice

2000 ◽  
Vol 21 ◽  
pp. 225
Author(s):  
Jochen Wolfgang Herms ◽  
Ilka Schneider ◽  
Dieder Moechars ◽  
Martine Gilis ◽  
Cuno Kuiperi ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Hippocampal Neurons ◽  
Presenilin 1

scholarly journals Steroidogenic Factor-1 Controls the Aldose Reductase akr1b7 Gene Promoter in Transgenic Mice through an Atypical Binding Site

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2111-2120 ◽  
Author(s):  
Antoine Martinez ◽  
Pierre Val ◽  
Isabelle Sahut-Barnola ◽  
Christelle Aigueperse ◽  
Georges Veyssière ◽  
...  
Keyword(s):  
Gene Expression ◽  
Androgen Receptor ◽  
Transgenic Mice ◽  
Vas Deferens ◽  
Hormonal Control ◽  
Developmental Expression ◽  
Wild Type ◽  
Mouse Vas Deferens ◽  
Steroidogenic Factor 1

Aldo-keto-reductase 1B7/mouse vas deferens protein (AKR1B7/MVDP) is expressed in rodent steroidogenic glands and in the mouse vas deferens. In steroidogenic organs, AKR1B7/MVDP scavenges isocaproaldehyde produced from the cholesterol side-chain cleavage reaction. Akr1b7/mvdp is responsive to ACTH in adrenals and to androgens in vas deferens. Using transgenic mice, we previously delimited the regulatory DNA sequences necessary for expression in both organs and identified by cell transfections, a cryptic steroidogenic factor-1 (SF-1) response element (SFRE) at −102 that overlaps a proximal androgen-responsive element. To address its in vivo functions in adrenals, we devised a transgenic mouse study using wild-type and mutant akr1b7 promoters driving the chloramphenol acetyltransferase reporter gene. Adrenal expression in adults was impaired in all lines mutant for −102 SFRE. This effect is linked to impaired SF-1 binding and not to impaired androgen receptor binding, because akr1b7 expression is not affected in adrenals of androgen receptor-defective Tfm mice. Triphasic developmental patterns of both AKR1B7 and wild-type transgene expression paralleled changes in SF-1 levels/binding activity; expression was maximal in late embryos, minimal in 6- to 15-d-old neonates, and thereafter progressively restored. Differences in developmental expression between wild-type and mutant transgenes revealed that requirement for the −102 SFRE appears stage specific, as its integrity is an absolute prerequisite for reinduction of gene expression after postnatal d 15. Further, mutation of this site did not affect transgene responsiveness to ACTH. These findings demonstrate a new function for SFRE in vivo, via influencing promoter sensibility to postnatal changes of SF-1 contents, in controlling promoter strength in adults without affecting adrenal targeting, hormonal control, or early gene expression.

scholarly journals Chimeric rat/human neurotensin receptors localize a region of the receptor sensitive to binding of a novel, species-specific picomolar affinity peptide

1996 ◽  
Vol 271 (36) ◽  
pp. 22280
Author(s):  
Bernadette Cusak ◽  
Karen Groshan ◽  
Daniel J. McCormick ◽  
Yuan-Ping Pang ◽  
Robin Perry ◽  
...  
Keyword(s):  
Novel Species ◽  
Neurotensin Receptors ◽  
Affinity Peptide ◽  
Species Specific

scholarly journals Chronic alcohol exposure inhibits biotin uptake by pancreatic acinar cells: possible involvement of epigenetic mechanisms

2014 ◽  
Vol 307 (9) ◽  
pp. G941-G949 ◽  
Author(s):  
Padmanabhan Srinivasan ◽  
Rubina Kapadia ◽  
Arundhati Biswas ◽  
Hamid M. Said
Keyword(s):  
Transgenic Mice ◽  
Chronic Exposure ◽  
Methylation Status ◽  
Acinar Cells ◽  
Alcohol Exposure ◽  
Significant Inhibition ◽  
Pancreatic Acinar Cells ◽  
Chronic Alcohol ◽  
Wild Type ◽  
Chronic Alcohol Exposure

Chronic exposure to alcohol affects different physiological aspects of pancreatic acinar cells (PAC), but its effect on the uptake process of biotin is not known. We addressed this issue using mouse-derived pancreatic acinar 266-6 cells chronically exposed to alcohol and wild-type and transgenic mice (carrying the human SLC5A6 5′-promoter) fed alcohol chronically. First we established that biotin uptake by PAC is Na+ dependent and carrier mediated and involves sodium-dependent multivitamin transporter (SMVT). Chronic exposure of 266-6 cells to alcohol led to a significant inhibition in biotin uptake, expression of SMVT protein, and mRNA as well as in the activity of the SLC5A6 promoter. Similarly, chronic alcohol feeding of wild-type and transgenic mice carrying the SLC5A6 promoter led to a significant inhibition in biotin uptake by PAC, as well as in the expression of SMVT protein and mRNA and the activity of the SLC5A6 promoters expressed in the transgenic mice. We also found that chronic alcohol feeding of mice is associated with a significant increase in the methylation status of CpG islands predicted to be in the mouse Slc5a6 promoters and a decrease in the level of expression of transcription factor KLF-4, which plays an important role in regulating SLC5A6 promoter activity. These results demonstrate, for the first time, that chronic alcohol exposure negatively impacts biotin uptake in PAC and that this effect is exerted (at least in part) at the level of transcription of the SLC5A6 gene and may involve epigenetic/molecular mechanisms.

scholarly journals Pig zona pellucida 2 (pZP2) protein does not participate in zona pellucida formation in transgenic mice

Reproduction ◽  
2006 ◽  
Vol 132 (3) ◽  
pp. 455-464 ◽  
Author(s):  
Akiko Hasegawa ◽  
Nozomi Kanazawa ◽  
Hideaki Sawai ◽  
Shinji Komori ◽  
Koji Koyama
Keyword(s):  
Extracellular Matrix ◽  
Transgenic Mice ◽  
Molecular Species ◽  
Zona Pellucida ◽  
Transgenic Protein ◽  
Specific Manner ◽  
Species Specific ◽  
Deficient Mice

The zona pellucida, an extracellular matrix surrounding mammalian oocytes, is composed of three or four glycoproteins. It is well known that the zona pellucida plays several critical roles during fertilization, but there is little knowledge about its formation. The purpose of this study is to examine whether a pig zona pellucida glycoprotein 2 (pZP2) would assemble with mouse zona pellucida. A transgene construct was prepared by placing a minigene encoding pZP2 downstream from the promoter of mouse ZP2. The result showed that the transgenic protein was synthesized in growing oocytes but not incorporated into the zona pellucida. Furthermore, the pZP2 transgene did not rescue the phenotype in ZP2-knockout zona-deficient mice. These results indicate that pZP2 does not participate in mouse zona pellucida formation and the zona pellucida is constituted from its component proteins in a molecular species-specific manner between mice and pigs.

scholarly journals Bisecting GlcNAc structure is implicated in suppression of stroma-dependent haemopoiesis in transgenic mice expressing N-acetylglucosaminyltransferase III

1998 ◽  
Vol 331 (3) ◽  
pp. 733-742 ◽  
Author(s):  
Masafumi YOSHIMURA ◽  
Yoshito IHARA ◽  
Tetsuo NISHIURA ◽  
Yu OKAJIMA ◽  
Megumu OGAWA ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Transgenic Mice ◽  
Stromal Cells ◽  
Bone Marrow Cells ◽  
Adherent Cell ◽  
Wild Type ◽  
Spleen Cells ◽  
Bisecting Glcnac ◽  
Marrow Cells

Several sugar structures have been reported to be necessary for haemopoiesis. We analysed the haematological phenotypes of transgenic mice expressing β-1,4 N-acetylglucosaminyltransferase III (GnT-III), which forms bisecting N-acetylglucosamine on asparagine-linked oligosaccharides. In the transgenic mice, the GnT-III activity was elevated in bone marrow, spleen and peripheral blood and in isolated mononuclear cells from these tissues, whereas no activity was found in these tissues of wild-type mice. Stromal cells after long-term cultures of transgenic-derived bone marrow and spleen cells also showed elevated GnT-III activity, compared with an undetectable activity in wild-type stromal cells. As judged by HPLC analysis, lectin blotting and lectin cytotoxicity assay, bisecting GlcNAc residues were increased on both blood cells and stromal cells from bone marrow and spleen in transgenic mice. The transgenic mice displayed spleen atrophy, hypocellular bone marrow and pancytopenia. Bone marrow cells and spleen cells from transgenic mice produced fewer haemopoietic colonies. After lethal irradiation followed by bone marrow transplantation, transgenic recipient mice showed pancytopenia compared with wild-type recipient mice. Bone marrow cells from transgenic donors gave haematological reconstitution at the same level as wild-type donor cells. In addition, non-adherent cell production was decreased in long-term bone marrow cell cultures of transgenic mice. Collectively these results indicate that the stroma-supported haemopoiesis is compromised in transgenic mice expressing GnT-III, providing the first demonstration that the N-glycans have some significant roles in stroma-dependent haemopoiesis.

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