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  • Hormonal and developmental regulation of DAX-1 expression in Sertoli cells. 8961266

    Mutations in the human DAX-1 gene lead to X-linked adrenal hypoplasia congenita and hypogonadotropic hypogonadism. DAX-1 has been proposed to play a role in steroidogenesis because it is highly expressed in adrenocortical and testicular Leydig cells and because loss-of-function mutations lead to low serum levels of steroid hormones. Recent reports of DAX-1 expression in hypothalamus and pituitary, however, suggest additional functions for this protein. Here we demonstrate that DAX-1 is expressed in Sertoli cells of rat testis. This expression is regulated during spermatogenesis and peaks during the androgen-sensitive phase of the spermatogenic cycle. In addition, we show that DAX-1 expression in Sertoli cells is regulated developmentally. Maximum levels are present in the rat between postnatal days 20 and 30, during the first spermatogenic wave. Moreover, we show that activation of the cAMP-signaling pathway by the pituitary hormone FSH leads to a potent down-regulation of DAX-1 expression in cultured Sertoli cells. This down-regulation requires transcription and de novo protein synthesis. Taken together, these data indicate that DAX-1 expression in Sertoli cells may influence the development of spermatogenic cells in response to steroid and pituitary hormones.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MABD398
    Nombre del producto:
    Anti-DAX-1, clone 2F4 Antibody

  • Social isolation during puberty affects female sexual behavior in mice. 25324747

    Exposure to stress during puberty can lead to long-term behavioral alterations in adult rodents coincident with sex steroid hormone-dependent brain remodeling and reorganization. Social isolation is a stress for social animals like mice, but little is known about the effects of such stress during adolescence on later reproductive behaviors. The present study examined sexual behavior of ovariectomized, estradiol and progesterone primed female mice that were individually housed from 25 days of age until testing at approximately 95 days, or individually housed from day 25 until day 60 (during puberty), followed by housing in social groups. Mice in these isolated groups were compared to females that were group housed throughout the experiment. Receptive sexual behaviors of females and behaviors of stimulus males were recorded. Females housed in social groups displayed greater levels of receptive behaviors in comparison to both socially isolated groups. Namely, social females had higher lordosis quotients (LQs) and more often displayed stronger lordosis postures in comparison to isolated females. No differences between female groups were observed in stimulus male sexual behavior suggesting that female "attractiveness" was not affected by their social isolation. Females housed in social groups had fewer cells containing immunoreactive estrogen receptor (ER) α in the anteroventral periventricular nucleus (AVPV) and in the ventromedial nucleus of the hypothalamus (VMH) than both isolated groups. These results suggest that isolation during adolescence affects female sexual behavior and re-socialization for 1 month in adulthood is insufficient to rescue lordosis behavior from the effects of social isolation during the pubertal period.
    Tipo de documento:
    Referencia
    Referencia del producto:
    06-935
    Nombre del producto:
    Anti-Estrogen Receptor α Antibody

  • The generation of induced pluripotent stem cells for macular degeneration as a drug screening platform: identification of curcumin as a protective agent for retinal pigme ... 25136316

    Age-related macular degeneration (AMD) is one retinal aging process that may lead to irreversible vision loss in the elderly. Its pathogenesis remains unclear, but oxidative stress inducing retinal pigment epithelial (RPE) cells damage is perhaps responsible for the aging sequence of retina and may play an important role in macular degeneration. In this study, we have reprogrammed T cells from patients with dry type AMD into induced pluripotent stem cells (iPSCs) via integration-free episomal vectors and differentiated them into RPE cells that were used as an expandable platform for investigating pathogenesis of the AMD and in-vitro drug screening. These patient-derived RPEs with the AMD-associated background (AMD-RPEs) exhibited reduced antioxidant ability, compared with normal RPE cells. Among several screened candidate drugs, curcumin caused most significant reduction of ROS in AMD-RPEs. Pre-treatment of curcumin protected these AMD-RPEs from H2O2-induced cell death and also increased the cytoprotective effect against the oxidative stress of H2O2 through the reduction of ROS levels. In addition, curcumin with its versatile activities modulated the expression of many oxidative stress-regulating genes such as PDGF, VEGF, IGFBP-2, HO1, SOD2, and GPX1. Our findings indicated that the RPE cells derived from AMD patients have decreased antioxidative defense, making RPE cells more susceptible to oxidative damage and thereby leading to AMD formation. Curcumin represented an ideal drug that can effectively restore the neuronal functions in AMD patient-derived RPE cells, rendering this drug an effective option for macular degeneration therapy and an agent against aging-associated oxidative stress.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB5922

  • GKAP orchestrates activity-dependent postsynaptic protein remodeling and homeostatic scaling. 23143515

    How does chronic activity modulation lead to global remodeling of proteins at synapses and synaptic scaling? Here we report that guanylate kinase-associated protein (GKAP; also known as SAPAP), a scaffolding molecule linking NMDA receptor-PSD-95 to Shank-Homer complexes, acts in these processes. Overexcitation removes GKAP from synapses via the ubiquitin-proteasome system, whereas inactivity induces synaptic accumulation of GKAP in rat hippocampal neurons. Bidirectional changes in synaptic GKAP amounts are controlled by specific CaMKII isoforms coupled to different Ca(2+) channels. CaMKIIα activated by the NMDA receptor phosphorylates GKAP Ser54 to induce polyubiquitination of GKAP. In contrast, CaMKIIβ activation via L-type voltage-dependent calcium channels promotes GKAP recruitment by phosphorylating GKAP Ser340 and Ser384, which uncouples GKAP from myosin Va motor complex. Overexpressing GKAP turnover mutants not only hampers activity-dependent remodeling of PSD-95 and Shank but also blocks bidirectional synaptic scaling. Therefore, activity-dependent turnover of PSD proteins orchestrated by GKAP is critical for homeostatic plasticity.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB397
    Nombre del producto:
    Anti-Glutamate Receptor 2 Antibody, extracellular, clone 6C4

  • MutS homologue hMSH5: recombinational DSB repair and non-synonymous polymorphic variants. 24023853

    Double-strand breaks (DSBs) constitute the most deleterious form of DNA lesions that can lead to genome alterations and cell death, and the vast majority of DSBs arise pathologically in response to DNA damaging agents such as ionizing radiation (IR) and chemotherapeutic agents. Recent studies have implicated a role for the human MutS homologue hMSH5 in homologous recombination (HR)-mediated DSB repair and the DNA damage response. In the present study, we show that hMSH5 promotes HR-based DSB repair, and this property resides in the carboxyl-terminal portion of the protein. Our results demonstrate that DSB-triggered hMSH5 chromatin association peaks at the proximal regions of the DSB and decreases gradually with increased distance from the break. Furthermore, the DSB-triggered hMSH5 chromatin association is preceded by and relies on the assembly of hMRE11 and hRad51 at the proximal regions of the DSB. Lastly, the potential effects of hMSH5 non-synonymous variants (L85F, Y202C, V206F, R351G, L377F, and P786S) on HR and cell survival in response to DSB-inducing anticancer agents have been analyzed. These experiments show that the expression of hMSH5 variants elicits different survival responses to anticancer drugs cisplatin, bleomycin, doxorubicin and camptothecin. However, the effects of hMSH5 variants on survival responses to DSB-inducing agents are not directly correlated to their effects exerted on HR-mediated DSB repair, suggesting that the roles of hMSH5 variants in the processes of DNA damage response and repair are multifaceted.
    Tipo de documento:
    Referencia
    Referencia del producto:
    17-371
    Nombre del producto:
    EZ-ChIP™

  • Enhanced nerve-stimulated muscarinic and neurokinin contractions of ileum from streptozotocin guinea-pigs. 22676206

    Diabetes mellitus can lead to neuropathy of enteric neurons, resulting in abnormal gut motility. These studies investigated voltage-dependent contributions of muscarinic M(3) receptor activation by acetylcholine and neurokinin NK(1) receptor activation by neurokinins to nerve-stimulated contractions of longitudinal ileal strips from STZ guinea-pigs, a type 1 diabetic model with insulin deficiency, but mild hyperglycaemia. Contractions to bethanechol, substance P methyl ester, and nerve stimulation were greater in diabetic as compared to control ileum. The muscarinic M(3) receptor antagonist 4-DAMP at lower voltages and the neurokinin NK(1) receptor antagonist SR140333 at higher voltages, but not the neurokinin NK(1) receptor antagonist CP-96,345, were more effective at inhibiting nerve-stimulated immediate peak contractions and total areas of contraction of ileum from diabetic as compared to control animals. For diabetic ileum, voltage-dependent increases in the areas of nerve-stimulated contraction were observed in the presence of 4-DAMP and CP-96,345 but not SR140333. At low voltages only, nerve-stimulated release of acetylcholine was greater from diabetic as compared to control ileum. Fluorescence intensity of tachykinin-like immunoreactivity was increased in ileal myenteric ganglia from diabetic as compared to control animals. In diabetic guinea-pigs, stronger ileal nerve-stimulated contractions reflected increased release of acetylcholine at lower voltages and tachykinins at higher voltages, as well as increased sensitivity of smooth muscle M(3) and NK(1) receptors to acetylcholine and tachykinins. Hypoinsulinaemia may be a primary contributor to intestinal motility dysfunction in type 1 diabetes mellitus.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB962

  • Central auditory plasticity after carboplatin-induced unilateral inner ear damage in the chinchilla: Up-regulation of GAP-43 in the ventral cochlear nucleus. 19435600

    Inner ear damage may lead to structural changes in the central auditory system. In rat and chinchilla, cochlear ablation and noise trauma result in fiber growth and synaptogenesis in the ventral cochlear nucleus (VCN). In this study, we documented the relationship between carboplatin-induced hair cell degeneration and VCN plasticity in the chinchilla. Unilateral application of carboplatin (5mg/ml) on the round window membrane resulted in massive hair cell loss. Outer hair cell degeneration showed a pronounced basal-to-apical gradient while inner hair cell loss was more equally distributed throughout the cochlea. Expression of the growth associated protein GAP-43, a well-established marker for synaptic plasticity, was up-regulated in the ipsilateral VCN at 15 and 31 days post-carboplatin, but not at 3 and 7 days. In contrast, the dorsal cochlear nucleus showed only little change. In VCN, the high-frequency area dorsally showed slightly yet significantly stronger GAP-43 up-regulation than the low-frequency area ventrally, possibly reflecting the high-to-low frequency gradient of hair cell degeneration. Synaptic modification or formation of new synapses may be a homeostatic process to re-adjust mismatched inputs from two ears. Alternatively, massive fiber growth may represent a deleterious process causing central hyperactivity that leads to loudness recruitment or tinnitus.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB347
    Nombre del producto:
    Anti-Growth Associated Protein 43 Antibody, clone 9-1E12

  • Cell cycle arrest at the initiation step of human chromosomal DNA replication causes DNA damage. 15456844

    Cell cycle arrest in response to environmental effects can lead to DNA breaks. We investigated whether inhibition of DNA replication during the initiation step can lead to DNA damage and characterised a cell-cycle-arrest point at the replication initiation step before the establishment of active replication forks. This arrest can be elicited by the iron chelators mimosine, ciclopirox olamine or 2,2'-bipyridyl, and can be reversed by the removal of the drugs or the addition of excess iron. Iron depletion induces DNA double-strand breaks in treated cells, and activates a DNA damage response that results in focal phosphorylation of histone H2AX, focal accumulation of replication protein A (RPA) and ATR (ATM and Rad3-related kinase), and activation of CHK1 kinase. Abrogation of the checkpoint response does not abolish the cell cycle arrest before the establishment of active DNA replication forks. DNA breaks appear concomitantly with the arrival of cells at the arrest point and persist upon release from the cell cycle block. We conclude that DNA double-strand breaks are the consequence, and not the cause, of cell cycle arrest during the initiation step of DNA replication by iron chelation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    07-164
    Nombre del producto:
    Anti-phospho-H2A.X (Ser139) Antibody

  • Upregulation of Semaphorin 3A and the associated biochemical and cellular events in a rat model of retinal detachment. 18815803

    BACKGROUND: Retinal detachment, as a result of injury or disease, is a severe disorder that may ultimately lead to complete blindness. Despite advanced surgical repair techniques, the visual acuity of patients is often limited. We investigated some of the biochemical and morphological alterations following experimental retinal detachment in laboratory animals. METHODS: Unilateral retinal detachment was induced in male Wistar rats; contralateral untreated eyes served as a control. Approximately half of the retinal area was detached by a sub-retinal injection of 5 mul Saline. The incidence and extent of the retinal detachment was evaluated using MRI analysis and fundus images. The retinas were collected at intervals of 24 hours, 7, 14 and 28 days following the procedure. Using Western blot and immunohistochemical analysis, the expression levels of Semaphorin3A, Neuropilin1, GAP43 and NF-H were studied. In addition, morphological changes in Müller and microglial cells were examined. TUNEL staining was used to assess apoptosis. RESULTS: We found that the expression level of Semaphorin3A was up-regulated and reached its peak at two time points: 24 hours and 14 days after surgery. A similar pattern of expression was found for Neuropilin1. TUNEL-positive cells, indicating apoptotic processes, were evident 24 hours post retinal detachment and increased after 7 days. On the other hand, GAP43 expression was up-regulated 14 days after retinal detachment, and further intensified 28 days post-surgery. Microglial cells were activated shortly after detachment and concentrated mostly at the inner plexiform layer. GFAP staining revealed hypertrophy of Müller cells. CONCLUSIONS: The biochemical and morphological changes suggest that apoptosis as well as axonal regrowth take place following retinal detachment. Collectively, these findings may explain the limited success following repair surgery in terms of visual acuity and physiological function of the retina. Our study may open a new approach for treatment of early phase retinal detachment, as well as improve post-operative care that may, in turn, improve the functional result of the surgery. In addition, further study is required on several other factors that may affect visual acuity, such as size and location of the detached area and the time lapse between detachment and surgery.
    Tipo de documento:
    Referencia
    Referencia del producto:
    S7110
    Nombre del producto:
    ApopTag® Fluorescein In Situ Apoptosis Detection Kit

  • Sodium butyrate induced structural changes in HeLa cell chromatin. 7074068

    Postsynthetic modifications of core histones by treatment of HeLa S3 cells with 5mM sodium butyrate lead to alterations in the structure of high molecular weight chromatin. Whole chromatin from butyrate-treated cells, which results in highly acetylated core histones, has an ellipticity [theta]282.5 of 3700 deg cm2 dmol-1 (0.2 mM EDTA, pH 7.4) that is 1200 deg c m2 dmol-1 less than chromatin from untreated HeLa cells, suggesting a more condensed structure. No difference in the circular dichroism spectra was observed in H1-stripped, high molecular weight chromatin obtained from control and butyrate-treated cells at low (0.2 mM EDTA, pH 7.4) ionic strength. Thermal denaturation profiles of high molecular weight chromatin were resolved into three transitions and exhibited a shifting of hyperchromicity from transition I to transitions III, at a higher Tm, with butyrate treatment of HeLa cells, further indicating a more compact structure. Thermal denaturation profiles of H1-stripped chromatin were not affected by butyrate treatment. Ionic strength studies in the range of 0-5 mM NaH2PO4, 0.2 mM EDTA, pH 7.4, of high molecular weight chromatin exhibited a decrease in [theta]282.5 and a shifting of hyperchromicity from transition I to transition III with increasing ionic strength. Control high molecular weight chromatin was more sensitive to changes in ionic strength than its highly acetylated counterpart. These results suggest that acetylation of histones alone does not result in a change in histone-DNA interactions but other changes associated with butyrate treatment most probably cause a more condensed structure, of the fraction studied herein, which is mediated by H1 or other materials removed during stripping in 0.35 M NaCl.
    Tipo de documento:
    Referencia
    Referencia del producto:
    06-598
    Nombre del producto:
    Anti-acetyl-Histone H4 Antibody