The Experts below are selected from a list of 138267 Experts worldwide ranked by ideXlab platform
Barak Blum - One of the best experts on this subject based on the ideXlab platform.
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Synaptotagmins Tweak Functional β Cell Maturation
Developmental cell, 2018Co-Authors: Jennifer M. Gilbert, Barak BlumAbstract:Immature β Cells secrete insulin at a lower glucose threshold compared to mature β Cells. In this issue of Developmental Cell, Huang et al. (2018) show that the increase in glucose threshold during β Cell Maturation is achieved through balance between the Ca2+-sensitive synaptotagmin 7 and the Ca2+-insensitive synaptotagmin 4.
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Functional beta-Cell Maturation is marked by an increased glucose threshold and by expression of urocortin 3
Nature Biotechnology, 2012Co-Authors: Barak Blum, Siniša Hrvatin, Christian Schuetz, Claire Bonal, Alireza Rezania, Douglas A MeltonAbstract:Insulin-expressing Cells that have been differentiated from human pluripotent stem Cells in vitro lack the glucose responsiveness characteristic of mature beta Cells. Beta-Cell Maturation in mice was studied to find genetic markers that enable screens for factors that induce bona fide beta Cells in vitro . We find that functional beta-Cell Maturation is marked by an increase in the glucose threshold for insulin secretion and by expression of the gene urocortin 3. Cultured human pluripotent stem Cells can be differentiated to immature pancreatic beta Cells, but no one has yet succeeded in maturing these Cells in vitro . Blum et al . define markers of beta-Cell Maturation that can be used to screen conditions for generating fully functional beta Cells.
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Functional beta-Cell Maturation is marked by an increased glucose threshold and by expression of urocortin 3
Nature biotechnology, 2012Co-Authors: Barak Blum, Siniša Hrvatin, Christian Schuetz, Claire Bonal, Alireza Rezania, Douglas A MeltonAbstract:Insulin-expressing Cells that have been differentiated from human pluripotent stem Cells in vitro lack the glucose responsiveness characteristic of mature beta Cells. Beta-Cell Maturation in mice was studied to find genetic markers that enable screens for factors that induce bona fide beta Cells in vitro. We find that functional beta-Cell Maturation is marked by an increase in the glucose threshold for insulin secretion and by expression of the gene urocortin 3.
Douglas A Melton - One of the best experts on this subject based on the ideXlab platform.
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Functional beta-Cell Maturation is marked by an increased glucose threshold and by expression of urocortin 3
Nature Biotechnology, 2012Co-Authors: Barak Blum, Siniša Hrvatin, Christian Schuetz, Claire Bonal, Alireza Rezania, Douglas A MeltonAbstract:Insulin-expressing Cells that have been differentiated from human pluripotent stem Cells in vitro lack the glucose responsiveness characteristic of mature beta Cells. Beta-Cell Maturation in mice was studied to find genetic markers that enable screens for factors that induce bona fide beta Cells in vitro . We find that functional beta-Cell Maturation is marked by an increase in the glucose threshold for insulin secretion and by expression of the gene urocortin 3. Cultured human pluripotent stem Cells can be differentiated to immature pancreatic beta Cells, but no one has yet succeeded in maturing these Cells in vitro . Blum et al . define markers of beta-Cell Maturation that can be used to screen conditions for generating fully functional beta Cells.
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Functional beta-Cell Maturation is marked by an increased glucose threshold and by expression of urocortin 3
Nature biotechnology, 2012Co-Authors: Barak Blum, Siniša Hrvatin, Christian Schuetz, Claire Bonal, Alireza Rezania, Douglas A MeltonAbstract:Insulin-expressing Cells that have been differentiated from human pluripotent stem Cells in vitro lack the glucose responsiveness characteristic of mature beta Cells. Beta-Cell Maturation in mice was studied to find genetic markers that enable screens for factors that induce bona fide beta Cells in vitro. We find that functional beta-Cell Maturation is marked by an increase in the glucose threshold for insulin secretion and by expression of the gene urocortin 3.
Irena Sokolnicka - One of the best experts on this subject based on the ideXlab platform.
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Common Variable Immune Deficiency in Children—Clinical Characteristics Varies Depending on Defect in Peripheral B Cell Maturation
Journal of Clinical Immunology, 2013Co-Authors: Barbara Piątosa, Małgorzata Pac, Katarzyna Siewiera, Barbara Pietrucha, Maja Klaudel-dreszler, Edyta Heropolitańska-pliszka, Beata Wolska-kuśnierz, Hanna Dmeńska, Hanna Gregorek, Irena SokolnickaAbstract:Common variable immune deficiency (CVID) is a heterogeneous disease associated with ineffective production of antibodies. It is usually diagnosed in adulthood, but a variable proportion of children develop CVID. Early identification of patients with potentially worse prognosis may help to avoid serious complications. The goal of this study was to associate the clinical phenotype of patients with early onset CVID with peripheral B-Cell Maturation profile. Four color flow cytometry was used to define distribution of peripheral B-Cell subsets in 49 children with early-onset CVID. All clinical data were extracted from medical records. A proportion of patients demonstrated diminishing with time total B-lymphocytes pool, beyond physiological age-related changes. Irrespective from duration of the follow-up period the B-Cell Maturation profile in individual patients remained unchanged. We identified six different aberrant peripheral B Cell Maturation profiles associated with different clinical characteristics. Patients with an early B-Cell Maturation block earlier required replacement therapy and were at significantly greater risk of enteropathy, granuloma formation, cytopenia, and lymphoproliferation. B-Cell Maturation inhibited at the natural effector stage was associated with higher risk of autoimmune manifestations other than autoimmune cytopenia. Prevalence of male patients was observed among patients with B-Cell Maturation inhibited at naïve B-Cell stage. In conclusion, the diagnostic process in patients with suspected early-onset CVID shall include routine analysis of peripheral B-Cell Maturation to provide surrogate markers identifying patients at greater risk of developing certain complications.
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Common variable immune deficiency in children--clinical characteristics varies depending on defect in peripheral B Cell Maturation.
Journal of clinical immunology, 2013Co-Authors: Barbara Piątosa, Małgorzata Pac, Katarzyna Siewiera, Barbara Pietrucha, Maja Klaudel-dreszler, Edyta Heropolitańska-pliszka, Beata Wolska-kuśnierz, Hanna Dmeńska, Hanna Gregorek, Irena SokolnickaAbstract:Common variable immune deficiency (CVID) is a heterogeneous disease associated with ineffective production of antibodies. It is usually diagnosed in adulthood, but a variable proportion of children develop CVID. Early identification of patients with potentially worse prognosis may help to avoid serious complications. The goal of this study was to associate the clinical phenotype of patients with early onset CVID with peripheral B-Cell Maturation profile. Four color flow cytometry was used to define distribution of peripheral B-Cell subsets in 49 children with early-onset CVID. All clinical data were extracted from medical records. A proportion of patients demonstrated diminishing with time total B-lymphocytes pool, beyond physiological age-related changes. Irrespective from duration of the follow-up period the B-Cell Maturation profile in individual patients remained unchanged. We identified six different aberrant peripheral B Cell Maturation profiles associated with different clinical characteristics. Patients with an early B-Cell Maturation block earlier required replacement therapy and were at significantly greater risk of enteropathy, granuloma formation, cytopenia, and lymphoproliferation. B-Cell Maturation inhibited at the natural effector stage was associated with higher risk of autoimmune manifestations other than autoimmune cytopenia. Prevalence of male patients was observed among patients with B-Cell Maturation inhibited at naive B-Cell stage. In conclusion, the diagnostic process in patients with suspected early-onset CVID shall include routine analysis of peripheral B-Cell Maturation to provide surrogate markers identifying patients at greater risk of developing certain complications.
Idit Shachar - One of the best experts on this subject based on the ideXlab platform.
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invariant chain induces b Cell Maturation by activating a tafii105 nf κb dependent transcription program
Journal of Biological Chemistry, 2001Co-Authors: Didi Matza, Orit Wolstein, Rivka Dikstein, Idit ShacharAbstract:Abstract Early stages of B Cell development occur in the bone marrow, resulting in formation of immature B Cells. From there these immature Cells migrate to the spleen where they differentiate to mature Cells. This final Maturation step is crucial for the B Cells to become responsive to antigens and to participate in the immune response. Recently, invariant chain (Ii), a major histocompatibility complex class II chaperone, as well as the transcription factors c-Rel and p65/RelA, were found to play a role in the final antigen-independent differentiation stage of B Cells in the spleen. In this study, we investigated a possible link between Ii-dependent B Cell Maturation and the NF-κB pathway. Our studies indicate that Ii-induced B Cell Maturation involves activation of transcription mediated by the NF-κB p65/RelA homodimer and requires the B Cell-enriched coactivator TBP-associated factorII105.
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Invariant Chain Induces B Cell Maturation by Activating a TAFII105-NF-κB-dependent Transcription Program
The Journal of biological chemistry, 2001Co-Authors: Didi Matza, Orit Wolstein, Rivka Dikstein, Idit ShacharAbstract:Abstract Early stages of B Cell development occur in the bone marrow, resulting in formation of immature B Cells. From there these immature Cells migrate to the spleen where they differentiate to mature Cells. This final Maturation step is crucial for the B Cells to become responsive to antigens and to participate in the immune response. Recently, invariant chain (Ii), a major histocompatibility complex class II chaperone, as well as the transcription factors c-Rel and p65/RelA, were found to play a role in the final antigen-independent differentiation stage of B Cells in the spleen. In this study, we investigated a possible link between Ii-dependent B Cell Maturation and the NF-κB pathway. Our studies indicate that Ii-induced B Cell Maturation involves activation of transcription mediated by the NF-κB p65/RelA homodimer and requires the B Cell-enriched coactivator TBP-associated factorII105.
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requirement for invariant chain in b Cell Maturation and function
Science, 1996Co-Authors: Idit Shachar, Richard A FlavellAbstract:Previously the role of invariant chain (Ii) had been described only as a chaperone that facilitates folding and transport of major histocompatability complex class II molecules; here it is shown that Ii is required for B Cell development. B Cells from mice lacking Ii were found to have a low response to T-independent type II antigen and could not proliferate after the mice were injected with antigen. Study of Cell surface markers revealed a developmental arrest that prevented immature virgin B Cells from becoming mature B Cells in the periphery. This block was independent of major histocompatability complex class II expression and was an intrinsic feature of B Cells that correlated with the amount of Ii. Thus, Ii participates by an unknown mechanism in B Cell Maturation.
Xavier Remesar - One of the best experts on this subject based on the ideXlab platform.
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Changes in alanine and glutamine transport during rat red blood Cell Maturation.
Bioscience reports, 1992Co-Authors: Antonio Felipe, Octavi Viñas, Xavier RemesarAbstract:Alanine and glutamine transport have been studied during red blood Cell Maturation in the rat. Kinetic parameters of Na+-dependent L-alanine transport were:K m 0.43 and 1.88 mM andV max 158 and 45 nmoles/ml ICW/min for reticulocytes and erythrocytes, respectively. During red Cell Maturation in the rat there is a loss of capacity and affinity of the system ASC for L-alanine transport. The values for Na+-dependent L-glutamine transport in reticulocytes wereK m 0.51 mM andV max 157 nmoles/ml ICW/min. On the other hand, a total loss of L-glutamine transport mediated by both N and ASC systems is demonstrated in mature red Cells. This seems to indicate that during rat red Cell Maturation the system N disappears. Furthermore, the system ASC specificity in mature Cells changes, and glutamine enters the red Cell by non-mediated diffusion processes.