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Article: Protein Kinase C-Dependent Effects of Neurosteroids on Synaptic GABA

Littlejohn, Erica L / Boychuk, Carie R

2021 Volume 12, Page(s) 742838

Abstract: The dorsal motor nucleus of the vagus (DMV) contains preganglionic motor neurons important for interpreting sensory input from the periphery, integrating that information, and coding the appropriate parasympathetic (vagal) output to target organs. ... ...

Abstract	The dorsal motor nucleus of the vagus (DMV) contains preganglionic motor neurons important for interpreting sensory input from the periphery, integrating that information, and coding the appropriate parasympathetic (vagal) output to target organs. Despite the critical role of hormonal regulation of vagal motor output, few studies examine the role of neurosteroids in the regulation of the DMV. Of the few examinations, no studies have investigated the potential impact of allopregnanolone (Allo), a neuroactive progesterone-derivative, in the regulation of neurotransmission on the DMV. Since DMV neuronal function is tightly regulated by GABA
Language	English
Publishing date	2021-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.742838
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Article ; Online: Determinants of Inequities in Neurologic Disease, Health, and Well-being: The NINDS Social Determinants of Health Framework.

Griffith, Derek M / Towfighi, Amytis / Manson, Spero M / Littlejohn, Erica L / Skolarus, Lesli E

Neurology

2023 Volume 101, Issue 7 Suppl 1, Page(s) S75–S81

Abstract: A National Institute of Neurological Disorders and Stroke working group developed the Determinants of Inequities in Neurological Disease, Health, and Well-being framework. Our goal was to guide and inspire a new generation of neurologic research that ... ...

Abstract	A National Institute of Neurological Disorders and Stroke working group developed the Determinants of Inequities in Neurological Disease, Health, and Well-being framework. Our goal was to guide and inspire a new generation of neurologic research that pushes the field to design and test new approaches in pursuit of health equity, population health, and social justice. We seek to expand the lens of those looking to reduce or eliminate racial, socioeconomic status, and other inequities in neurologic disease, health, and well-being to improve our collective ability to create research, programs, and policies that lead to larger, more impactful, and more sustainable change in neurologic disease patterns. In this context, we outline a framework that includes and highlights "upstream" factors in the hopes of enhancing the focus of research, programmatic, and policy efforts to reduce and eliminate inequities in neurologic health and well-being. We explicitly discuss racism and other structural factors to clarify that social determinants are not natural and unchangeable. Populations with a disproportionate burden of neurologic disease are not inherently deficient, despite what some approaches to framing health inequities imply. The framework is presented linearly, but the pathways linking the determinants of neurologic disease, health, and well-being are far more complex than those demonstrated by the arrows included in the figure. The framework highlights the different levels and scale of causation, including the structural and intermediary social determinants and their impact on neurologic health. We offer this framework to refine efforts to contextualize the interpretation of neurologic research findings and suggest new avenues for their application. We illustrate how behavioral and biological factors occur in a social and economic context, factors that have been understudied as points of intervention to reduce inequities in neurologic disease. Considering social and structural determinants of health provides promising new opportunities to achieve neurologic health equity, reach social justice, and improve our science. Extending our work in this fashion is not simply about health equity or social justice but to fundamentally improve the quality of neurologic research by enhancing underlying theory and improving study design and implementation.
MeSH term(s)	United States/epidemiology ; Humans ; Health Policy ; Social Determinants of Health ; National Institute of Neurological Disorders and Stroke (U.S.) ; Social Class ; Health Status Disparities
Language	English
Publishing date	2023-08-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000207566
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Article ; Online: Sex-steroid-dependent plasticity of brain-stem autonomic circuits.

Littlejohn, Erica L / Fedorchak, Stephanie / Boychuk, Carie R

American journal of physiology. Regulatory, integrative and comparative physiology

2020 Volume 319, Issue 1, Page(s) R60–R68

Abstract: In the central nervous system (CNS), nuclei of the brain stem play a critical role in the integration of peripheral sensory information and the regulation of autonomic output in mammalian physiology. The nucleus tractus solitarius of the brain stem acts ... ...

Abstract	In the central nervous system (CNS), nuclei of the brain stem play a critical role in the integration of peripheral sensory information and the regulation of autonomic output in mammalian physiology. The nucleus tractus solitarius of the brain stem acts as a relay center that receives peripheral sensory input from vagal afferents of the nodose ganglia, integrates information from within the brain stem and higher central centers, and then transmits autonomic efferent output through downstream premotor nuclei, such as the nucleus ambiguus, the dorsal motor nucleus of the vagus, and the rostral ventral lateral medulla. Although there is mounting evidence that sex and sex hormones modulate autonomic physiology at the level of the CNS, the mechanisms and neurocircuitry involved in producing these functional consequences are poorly understood. Of particular interest in this review is the role of estrogen, progesterone, and 5α-reductase-dependent neurosteroid metabolites of progesterone (e.g., allopregnanolone) in the modulation of neurotransmission within brain-stem autonomic neurocircuits. This review will discuss our understanding of the actions and mechanisms of estrogen, progesterone, and neurosteroids at the cellular level of brain-stem nuclei. Understanding the complex interaction between sex hormones and neural signaling plasticity of the autonomic nervous system is essential to elucidating the role of sex in overall physiology and disease.
MeSH term(s)	Animals ; Autonomic Nervous System/physiology ; Brain Stem/physiology ; Female ; Gonadal Steroid Hormones/physiology ; Humans ; Male ; Nerve Net/physiology ; Neuronal Plasticity/physiology
Chemical Substances	Gonadal Steroid Hormones
Language	English
Publishing date	2020-06-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00357.2019
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Article ; Online: Insulin-like growth factor-1 overexpression increases long-term survival of posttrauma-born hippocampal neurons while inhibiting ectopic migration following traumatic brain injury.

Littlejohn, Erica L / Scott, Danielle / Saatman, Kathryn E

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 46

Abstract: Cellular damage associated with traumatic brain injury (TBI) manifests in motor and cognitive dysfunction following injury. Experimental models of TBI reveal cell death in the granule cell layer (GCL) of the hippocampal dentate gyrus acutely after injury. ...

Abstract	Cellular damage associated with traumatic brain injury (TBI) manifests in motor and cognitive dysfunction following injury. Experimental models of TBI reveal cell death in the granule cell layer (GCL) of the hippocampal dentate gyrus acutely after injury. Adult-born neurons residing in the neurogenic niche of the GCL, the subgranular zone, are particularly vulnerable. Injury-induced proliferation of neural progenitors in the subgranular zone supports recovery of the immature neuron population, but their development and localization may be altered, potentially affecting long-term survival. Here we show that increasing hippocampal levels of insulin-like growth factor-1 (IGF1) is sufficient to promote end-stage maturity of posttrauma-born neurons and improve cognition following TBI. Mice with conditional overexpression of astrocyte-specific IGF1 and wild-type mice received controlled cortical impact or sham injury and bromo-2'-deoxyuridine injections for 7d after injury to label proliferating cells. IGF1 overexpression increased the number of GCL neurons born acutely after trauma that survived 6 weeks to maturity (NeuN+BrdU+), and enhanced their outward migration into the GCL while significantly reducing the proportion localized ectopically to the hilus and molecular layer. IGF1 selectively affected neurons, without increasing the persistence of posttrauma-proliferated glia in the dentate gyrus. IGF1 overexpressing animals performed better during radial arm water maze reversal testing, a neurogenesis-dependent cognitive test. These findings demonstrate the ability of IGF1 to promote the long-term survival and appropriate localization of granule neurons born acutely after a TBI, and suggest these new neurons contribute to improved cognitive function.
MeSH term(s)	Animals ; Behavior, Animal ; Brain Injuries, Traumatic/genetics ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/pathology ; Brain Injuries, Traumatic/physiopathology ; Cell Movement/genetics ; Cell Survival/genetics ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Hippocampus/metabolism ; Hippocampus/pathology ; Insulin-Like Growth Factor I/genetics ; Maze Learning ; Mice ; Mice, Transgenic ; Neural Stem Cells ; Neurogenesis/genetics ; Neurons/metabolism ; Neurons/pathology
Chemical Substances	Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2020-04-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-00925-6
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Article ; Online: Giving voice to Black women in science and medicine.

Ighodaro, Eseosa T / Littlejohn, Erica L / Akhetuamhen, Adesuwa I / Benson, Richard

Nature medicine

2021 Volume 27, Issue 8, Page(s) 1316–1317

MeSH term(s)	African Americans ; Biomedical Research ; Community-Institutional Relations ; Female ; Humans ; Medicine ; Voice
Language	English
Publishing date	2021-07-12
Publishing country	United States
Document type	Letter
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-021-01438-y
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Article ; Online: Early central cardiovagal dysfunction after high fat diet in a murine model.

Strain, Misty M / Espinoza, Liliana / Fedorchak, Stephanie / Littlejohn, Erica L / Andrade, Mary Ann / Toney, Glenn M / Boychuk, Carie R

Scientific reports

2023 Volume 13, Issue 1, Page(s) 6550

Abstract: High fat diet (HFD) promotes cardiovascular disease and blunted cardiac vagal regulation. Temporal onset of loss of cardiac vagal control and its underlying mechanism are presently unclear. We tested our hypothesis that reduced central vagal regulation ... ...

Abstract	High fat diet (HFD) promotes cardiovascular disease and blunted cardiac vagal regulation. Temporal onset of loss of cardiac vagal control and its underlying mechanism are presently unclear. We tested our hypothesis that reduced central vagal regulation occurs early after HFD and contributes to poor cardiac regulation using cardiovascular testing paired with pharmacology in mice, molecular biology, and a novel bi-transgenic mouse line. Results show HFD, compared to normal fat diet (NFD), significantly blunted cardio/pulmonary chemoreflex bradycardic responses after 15 days, extending as far as tested (> 30 days). HFD produced resting tachycardia by day 3, reflected significant loss of parasympathetic tone. No differences in bradycardic responses to graded electrical stimulation of the distal cut end of the cervical vagus indicated diet-induced differences in vagal activity were centrally mediated. In nucleus ambiguus (NA), surface expression of δ-subunit containing type A gamma-aminobutyric acid receptors (GABA
MeSH term(s)	Mice ; Animals ; Disease Models, Animal ; Diet, High-Fat/adverse effects ; Medulla Oblongata/metabolism ; Vagus Nerve/physiology ; Bradycardia ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2023-04-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-32492-w
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Article ; Online: Advancing Health Equity in Neurologic Disorders and Stroke: Stakeholder Insights Into Health Disparities, Research Gaps, and Potential Interventions.

Littlejohn, Erica L / Booker, Naomi E / Chambers, Stacey / Akinsanya, Jemima A / Sankar, Cheryse A / Benson, Richard T

Neurology

2023 Volume 101, Issue 7 Suppl 1, Page(s) S92–S103

Abstract: Objectives: The purpose of this study was to analyze the National Institute of Neurological Disorders and Stroke (NINDS) Request for Information (RFI) input from the public-including health care providers, researchers, patients, patient advocates, ... ...

Abstract	Objectives: The purpose of this study was to analyze the National Institute of Neurological Disorders and Stroke (NINDS) Request for Information (RFI) input from the public-including health care providers, researchers, patients, patient advocates, caregivers, advocacy organizations, professional societies, and private and academic stakeholders with an interest in health disparities (HDs) in neurologic disease. RFI questions were structured to solicit input on what stakeholders believe are neurologic disease HD research priorities, drivers of health inequity, and potential interventions. Furthermore, these stakeholder insights were examined within the context of contemporary scientific literature and research frameworks on health equity and health disparities. Background: The NINDS published a RFI from March 31 to July 15, 2020. The RFI analysis presented here is part of a larger strategic planning process aimed to guide future NINDS efforts in neurologic disorder health equity (HE) research and training. The public commented on facilitators of HDs, populations that experience HDs (HDPs), potential interventions, and research opportunities related to HDs in neurologic disease and/or care in the United States across the lifespan. Responses were analyzed using qualitative methodology. Frequently suggested interventions were thematically clustered using the interpretive phenomenological analysis methodology and are presented in this article to provide a stakeholder-identified roadmap for advancing HE. Results: Respondents identified socioecological factors as driving HDs in 89% of determinants reported. Stakeholder-reported HD determinants and subsequent interventions could be classified into the following conceptual categories: HDP neurospecialty care access, innovative HDP engagement and research inclusion strategies, and development of a well-trained clinician-scientist HD workforce. Clustering of the feedback from patient and patient-adjacent respondents (i.e., caretakers and patient advocates) highlighted the prevalence of patient-provider interpersonal factors and limited resources driving access-to-care barriers among their sentiments. Discussion: Respondent sentiments suggest prioritization of social determinants of health (SDOH) research, shifting away from the common target of biological and behavioral themes addressed in the existing body of HE research provided by the stakeholder. Overall, respondents suggest focusing research prioritization on access to care, engagement across the HE research and care landscape, and HE workforce development.
MeSH term(s)	Humans ; United States ; Evidence Gaps ; Health Equity ; Nervous System Diseases/epidemiology ; Nervous System Diseases/therapy ; Stroke/epidemiology ; Stroke/therapy ; Caregivers
Language	English
Publishing date	2023-08-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000207570
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Article: IGF1-Stimulated Posttraumatic Hippocampal Remodeling Is Not Dependent on mTOR.

Littlejohn, Erica L / DeSana, Anthony J / Williams, Hannah C / Chapman, Rudy T / Joseph, Binoy / Juras, Jelena A / Saatman, Kathryn E

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 663456

Abstract: Adult hippocampal neurogenesis is stimulated acutely following traumatic brain injury (TBI). However, many hippocampal neurons born after injury develop abnormally and the number that survive long-term is debated. In experimental TBI, insulin-like growth ...

Abstract	Adult hippocampal neurogenesis is stimulated acutely following traumatic brain injury (TBI). However, many hippocampal neurons born after injury develop abnormally and the number that survive long-term is debated. In experimental TBI, insulin-like growth factor-1 (IGF1) promotes hippocampal neuronal differentiation, improves immature neuron dendritic arbor morphology, increases long-term survival of neurons born after TBI, and improves cognitive function. One potential downstream mediator of the neurogenic effects of IGF1 is mammalian target of rapamycin (mTOR), which regulates proliferation as well as axonal and dendritic growth in the CNS. Excessive mTOR activation is posited to contribute to aberrant plasticity related to posttraumatic epilepsy, spurring preclinical studies of mTOR inhibitors as therapeutics for TBI. The degree to which pro-neurogenic effects of IGF1 depend upon upregulation of mTOR activity is currently unknown. Using immunostaining for phosphorylated ribosomal protein S6, a commonly used surrogate for mTOR activation, we show that controlled cortical impact TBI triggers mTOR activation in the dentate gyrus in a time-, region-, and injury severity-dependent manner. Posttraumatic mTOR activation in the granule cell layer (GCL) and dentate hilus was amplified in mice with conditional overexpression of IGF1. In contrast, delayed astrocytic activation of mTOR signaling within the dentate gyrus molecular layer, closely associated with proliferation, was not affected by IGF1 overexpression. To determine whether mTOR activation is necessary for IGF1-mediated stimulation of posttraumatic hippocampal neurogenesis, wildtype and IGF1 transgenic mice received the mTOR inhibitor rapamycin daily beginning at 3 days after TBI, following pulse labeling with bromodeoxyuridine. Compared to wildtype mice, IGF1 overexpressing mice exhibited increased posttraumatic neurogenesis, with a higher density of posttrauma-born GCL neurons at 10 days after injury. Inhibition of mTOR did not abrogate IGF1-stimulated enhancement of posttraumatic neurogenesis. Rather, rapamycin treatment in IGF1 transgenic mice, but not in WT mice, increased numbers of cells labeled with BrdU at 3 days after injury that survived to 10 days, and enhanced the proportion of posttrauma-born cells that differentiated into neurons. Because beneficial effects of IGF1 on hippocampal neurogenesis were maintained or even enhanced with delayed inhibition of mTOR, combination therapy approaches may hold promise for TBI.
Language	English
Publishing date	2021-05-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.663456
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Article ; Online: GABA

Littlejohn, Erica L / Espinoza, Liliana / Lopez, Monica M / Smith, Bret N / Boychuk, Carie R

Journal of neurophysiology

2019 Volume 122, Issue 5, Page(s) 2130–2141

Abstract: The dorsal motor nucleus of the vagus (DMV) contains the preganglionic motor neurons important in the regulation of glucose homeostasis and gastrointestinal function. Despite the role of sex in the regulation of these processes, few studies examine the ... ...

Abstract	The dorsal motor nucleus of the vagus (DMV) contains the preganglionic motor neurons important in the regulation of glucose homeostasis and gastrointestinal function. Despite the role of sex in the regulation of these processes, few studies examine the role of sex and/or ovarian cycle in the regulation of synaptic neurotransmission to the DMV. Since GABAergic neurotransmission is critical to normal DMV function, the present study used in vitro whole cell patch-clamping to investigate whether sex differences exist in GABAergic neurotransmission to DMV neurons. It additionally investigated whether the ovarian cycle plays a role in those sex differences. The frequency of phasic GABA
MeSH term(s)	3-Oxo-5-alpha-Steroid 4-Dehydrogenase/drug effects ; 3-Oxo-5-alpha-Steroid 4-Dehydrogenase/metabolism ; 5-alpha Reductase Inhibitors/pharmacology ; Animals ; Estrogens/metabolism ; Female ; Inhibitory Postsynaptic Potentials/drug effects ; Inhibitory Postsynaptic Potentials/physiology ; Male ; Menstrual Cycle/metabolism ; Mice ; Motor Neurons/metabolism ; Motor Neurons/physiology ; Neuronal Plasticity/physiology ; Ovariectomy ; Patch-Clamp Techniques ; Receptors, GABA-A/metabolism ; Sex Characteristics ; Vagus Nerve/metabolism ; Vagus Nerve/physiology ; gamma-Aminobutyric Acid
Chemical Substances	5-alpha Reductase Inhibitors ; Estrogens ; Receptors, GABA-A ; gamma-Aminobutyric Acid (56-12-2) ; 3-Oxo-5-alpha-Steroid 4-Dehydrogenase (EC 1.3.99.5)
Language	English
Publishing date	2019-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.00039.2019
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Article ; Online: PAX6 is expressed in pancreatic cancer and actively participates in cancer progression through activation of the MET tyrosine kinase receptor gene.

Mascarenhas, Joseph B / Young, Kacey P / Littlejohn, Erica L / Yoo, Brian K / Salgia, Ravi / Lang, Deborah

The Journal of biological chemistry

2009 Volume 284, Issue 40, Page(s) 27524–27532

Abstract: Tumors of the exocrine pancreas have a poor prognosis. Several proteins are overexpressed in this cancer type, including the MET tyrosine kinase receptor and the transcription factor PAX6. In this report, we find that PAX6(5a), an alternately spliced ... ...

Abstract	Tumors of the exocrine pancreas have a poor prognosis. Several proteins are overexpressed in this cancer type, including the MET tyrosine kinase receptor and the transcription factor PAX6. In this report, we find that PAX6(5a), an alternately spliced variant form of PAX6, is expressed in pancreatic carcinoma cell lines at higher levels than the canonical PAX6 protein. Both protein forms of PAX6 bind directly to an enhancer element in the MET promoter and activate the expression of the MET gene. In addition, inhibition of PAX6 transcripts leads to a decline in cell growth and survival, differentiation, and a concurrent reduction of MET protein expression. These data support a model for a neoplastic pathway, where expression of a transcription factor from development activates the MET receptor, a protein that has been directly linked to protumorigenic processes of resisting apoptosis, tumor growth, invasion, and metastasis.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Animals ; Apoptosis/genetics ; Base Sequence ; Cell Line, Tumor ; Disease Progression ; Eye Proteins/genetics ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Homeodomain Proteins/genetics ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Metastasis/genetics ; PAX6 Transcription Factor ; Paired Box Transcription Factors/deficiency ; Paired Box Transcription Factors/genetics ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Phenotype ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-met ; Receptors, Growth Factor/genetics ; Repressor Proteins/genetics ; Transcriptional Activation
Chemical Substances	Eye Proteins ; Homeodomain Proteins ; PAX6 Transcription Factor ; PAX6 protein, human ; Paired Box Transcription Factors ; Pax6 protein, mouse ; Proto-Oncogene Proteins ; Receptors, Growth Factor ; Repressor Proteins ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2009-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M109.047209
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