Neuronal Apoptosis-Inhibitory Protein
Spinal Muscular Atrophies of Childhood
Muscular Atrophy, Spinal
SMN Complex Proteins
Survival of Motor Neuron 1 Protein
Nerve Tissue Proteins
Gene Deletion
Cyclic AMP Response Element-Binding Protein
Apoptosis
Neurons
CASP8 and FADD-Like Apoptosis Regulating Protein
Caspase 3
Caspases
Attenuation of ischemia-induced cellular and behavioral deficits by X chromosome-linked inhibitor of apoptosis protein overexpression in the rat hippocampus. (1/101)
Transient forebrain ischemia produced by four-vessel occlusion (4-VO) triggers the delayed death of CA1 neurons in the hippocampus, resulting in behavioral deficits of spatial learning performance. We demonstrate that CA1 neuronal loss induced by 4-VO (12 min) is preceded by a selective and marked elevation of catalytically active caspase-3 in these neurons, indicative of apoptosis. Virally mediated overexpression of the anti-apoptotic gene X chromosome-linked inhibitor of apoptosis protein (XIAP) prevented both the production of catalytically active caspase-3 and degeneration of CA1 neurons after transient forebrain ischemia. CA1 neurons protected in this manner appeared to function normally, as assessed by immunohistochemical detection of the neuronal activity marker nerve growth factor inducible-A and by spatial learning performance in the Morris water maze. These findings indicate that caspase-3 activation is a key event in ischemic neuronal death and that blockade of this event by XIAP overexpression permits CA1 neurons to survive and operate properly after an ischemic insult. (+info)Prenatal diagnosis of spinal muscular atrophy type I (Werdnig- hoffmann) by DNA deletion analysis of cultivated amniocytes. (2/101)
AIM: Presentation of a prenatally diagnosed case of Werdnig-Hoffmann disease, the most severe type of spinal muscular atrophy. METHODS: DNA obtained from cultivated amniocytes was analyzed for deletions in the survival motor neuron gene and neuronal apoptosis inhibitory protein gene. RESULTS: The fetus was diagnosed as an affected homozygote for deletions in exon 7 and exon 8 of the survival motor neuron gene. No deletions of exon 5 in the neuronal apoptosis inhibitory protein gene were found. CONCLUSION: Direct DNA deletion analysis of the survival motor neuron gene and neuronal apoptosis inhibitory protein gene in affected families represents a highly reliable and fast method for prenatal diagnosis of Werdnig-Hoffmann disease. (+info)The neuronal apoptosis inhibitory protein (Naip) is expressed in macrophages and is modulated after phagocytosis and during intracellular infection with Legionella pneumophila. (3/101)
Legionella pneumophila is an intracellular pathogen that causes Legionnaires' disease in humans. Inbred mouse strains are uniformly resistant to L. pneumophila infection with the notable exception of A/J, where the chromosome 13 locus Lgn1 renders A/J macrophages permissive to L. pneumophila replication. The mouse Lgn1 region is syntenic with the spinal muscular atrophy (SMA) locus on human chromosome 5 and includes several copies of the neuronal apoptosis inhibitory protein (Naip) gene. We have analyzed a possible link among Lgn1, Naip, and macrophage function. RNA expression studies show that Naip (mostly copy 2) mRNA transcripts are expressed in macrophage-rich tissues, such as spleen, lung, and liver and are abundant in primary macrophages. Immunoblotting and immunoprecipitation analyses identify Naip protein expression in mouse macrophages and in macrophage cell lines RAW 264.7 and J774A. Interestingly, macrophages from permissive A/J mice express significantly less Naip protein than their nonpermissive C57BL/6J counterpart. Naip protein expression is increased after phagocytic events. Naip protein levels during infection with either virulent or avirulent strains of L. pneumophila increase during the first 6 h postinfection and remain elevated during the 48-h observation period. This enhanced expression is also observed in macrophages infected with Salmonella typhimurium. Likewise, an increase in Naip protein levels in macrophages is observed 24 h after phagocytosis of Latex beads. The cosegregation of Lgn1 and Naip together with the detected Naip protein expression in host macrophages as well as its modulation after phagocytic events and during intracellular infection make it an attractive candidate for the Lgn1 locus. (+info)The hippocampal neurons of neuronal apoptosis inhibitory protein 1 (NAIP1)-deleted mice display increased vulnerability to kainic acid-induced injury. (4/101)
The neuronal apoptosis inhibitory protein (NAIP) is a member of a novel family of inhibitor of apoptosis (IAP) proteins. The IAP genes are highly conserved from baculovirus to metazoans and suppress apoptosis induced by a variety of triggers both in vitro and in vivo. Here we describe the generation and characterization of mice with the targeted deletion of NAIP1. We demonstrate that the NAIP1-deleted mice develop normally. However, the survival of pyramidal neurons in the hippocampus after kainic acid-induced limbic seizures is greatly reduced in the NAIP1 knock-out animals. Thus, although NAIP1 is not necessary for normal development of murine central nervous system, the endogenous NAIP1 is required for neuronal survival in pathological conditions. (+info)Screening of deletions in SMN, NAIP and BTF2p44 genes in Turkish spinal muscular atrophy patients. (5/101)
Deletions of the spinal muscular atrophy (SMA)-determining gene, SMN1, NAIP, and a third multicopy gene, BTF2p44tel were investigated in 60 unrelated Turkish SMA patients. SMN1 was deleted for at least exons 7 and 8 in 85% of the Turkish SMA patients. The NAIP gene was deleted in 75 and 33% of type I and type II SMA patients, respectively. Analysis of the 5'end of the BTF2p44tel gene indicated the extension of deletion in 13.3% of the cases, mainly in type I patients. Deletions of the NAIP and BTF2p44tel genes were detected in 1.3 and 3.9% of carrriers, respectively, in Turkish SMA families. Two patients were detected to harbor the hybrid SMN gene, one type II with deletion of the NAIP gene, and one type III without deletion of the NAIP gene. (+info)Analysis of the SMN and NAIP genes in slovak spinal muscular atrophy patients. (6/101)
We identified homozygous absence of exon 7 of the telomeric copy of the survival motor neuron gene (telSMN) in 88.4% (38/43) of spinal muscular atrophy (SMA) patients from Slovakia. Additional deletions within the neuronal apoptosis inhibitory protein (NAIP) gene were found in 38.5% of type I, 12.5% of type II and never in type III SMA patients. Neither the SMN nor the NAIP gene was deleted in 81 healthy relatives and 25 controls tested. In one family, pseudodominant inheritance was identified. Both the type III SMA father and type II SMA son carried the homozygous deletion of the telSMN gene. One SMA I patient showed an SMN hybrid gene, probably created by intrachromosomal deletion. In two haploidentical type II SMA sibs, the telSMN exon 7 was absent on one chromosome, while the other carried an A-->G transition 96 bp upstream of exon 7 of the telSMN gene, a potential disease-causing mutation in these patients. (+info)Deletion of SMN and NAIP genes in Korean patients with spinal muscular atrophy. (7/101)
Childhood-onset proximal spinal muscular atrophies (SMAs) are an autosomal recessive, clinically heterogeneous group of neuronopathies characterized by selective degeneration of anterior horn cells. The causative genes to be reported are survival motor neuron (SMN) and neuronal apoptosis inhibitory protein (NAIP) genes. The deletion of telomeric copy of SMN (SMN(T)) gene was observed in over 95% of SMAs. The deletion rate of NAIP gene is 20-50% according to disease severity. The objective of this article is to genetically characterize the childhood-onset spinal muscular atrophy in Koreans. Five Korean families (14 constituents containing 5 probands) with SMA were included in this study. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were used for the deletion analysis of SMN(T). Multiplex PCR method was used for NAIP analysis. Four probands showed deletion of SMNT gene. Deletion of SMN(C) (centromeric SMN) gene was found in one proband who did not show the deletion of SMN(T) gene and in the father of one proband who showed the deletion of SMN(T) gene. The deletion of NAIP gene was not found among all the studied individuals. The extent of deletion in Koreans was smaller than that in other studied population. PCR-RFLP deletion analysis can be applied to diagnose SMA and make a prenatal diagnosis. (+info)NAIP interacts with hippocalcin and protects neurons against calcium-induced cell death through caspase-3-dependent and -independent pathways. (8/101)
Inhibitor-of-apoptosis proteins (IAPs), including neuronal apoptosis inhibitory protein (NAIP), inhibit cell death. Other IAPs inhibit key caspase proteases which effect cell death, but the mechanism by which NAIP acts is unknown. Here we report that NAIP, through its third baculovirus inhibitory repeat domain (BIR3), binds the neuron-restricted calcium-binding protein, hippocalcin, in an interaction promoted by calcium. In neuronal cell lines NSC-34 and Neuro-2a, over-expression of the BIR domains of NAIP (NAIP-BIR1-3) counteracted the calcium-induced cell death induced by ionomycin and thapsigargin. This protective capacity was significantly enhanced when NAIP-BIR1-3 was co-expressed with hippocalcin. Over-expression of the BIR3 domain or hippocalcin alone did not substantially enhance cell survival, but co-expression greatly increased their protective effects. These data suggest synergy between NAIP and hippocalcin in facilitating neuronal survival against calcium-induced death stimuli mediated through the BIR3 domain. Analysis of caspase activity after thapsigargin treatment revealed that caspase-3 is activated in NSC-34, but not Neuro-2a, cells. Thus NAIP, in conjunction with hippocalcin, can protect neurons against calcium-induced cell death in caspase-3-activated and non-activated pathways. (+info)NAIP (Neuronal Apoptosis Inhibitory Protein) is a protein involved in inhibiting programmed cell death, also known as apoptosis. It is a member of the inhibitor of apoptosis (IAP) family and is primarily expressed in neurons. NAIP plays a crucial role in preventing excessive cell death during nervous system development and after nerve injury. It functions by binding to and inhibiting certain caspases, which are enzymes that play an essential role in initiating and executing apoptosis. Mutations in the gene encoding NAIP have been associated with neurodegenerative disorders such as spinal muscular atrophy and amyotrophic lateral sclerosis (ALS).
Spinal muscular atrophies (SMAs) of childhood are a group of inherited neuromuscular disorders characterized by degeneration and loss of lower motor neurons in the spinal cord, leading to progressive muscle weakness and atrophy. The severity and age of onset can vary significantly, with some forms presenting in infancy and others in later childhood or even adulthood.
The most common form of SMA is 5q autosomal recessive SMA, also known as survival motor neuron (SMN) disease, which results from mutations in the SMN1 gene. The severity of this form can range from severe (type I or Werdnig-Hoffmann disease), intermediate (type II or chronic infantile neurodegenerative disorder), to mild (type III or Kugelberg-Welander disease).
Type I SMA is the most severe form, with onset before 6 months of age and rapid progression leading to death within the first two years of life if left untreated. Type II SMA has an onset between 6 and 18 months of age, with affected children never achieving the ability to walk independently. Type III SMA has a later onset, typically after 18 months of age, and is characterized by a slower progression, allowing for the ability to walk unaided, although mobility may be lost over time.
Other forms of childhood-onset SMA include autosomal dominant distal SMA, X-linked SMA, and spinal bulbar muscular atrophy (SBMA or Kennedy's disease). These forms have distinct genetic causes and clinical presentations.
In general, SMAs are characterized by muscle weakness, hypotonia, fasciculations, tongue atrophy, and depressed or absent deep tendon reflexes. Respiratory and nutritional support is often required in more severe cases. Recent advances in gene therapy have led to the development of disease-modifying treatments for some forms of SMA.
Spinal muscular atrophy (SMA) is a genetic disorder that affects the motor neurons in the spinal cord, leading to muscle weakness and atrophy. It is caused by a mutation in the survival motor neuron 1 (SMN1) gene, which results in a deficiency of SMN protein necessary for the survival of motor neurons.
There are several types of SMA, classified based on the age of onset and severity of symptoms. The most common type is type 1, also known as Werdnig-Hoffmann disease, which presents in infancy and is characterized by severe muscle weakness, hypotonia, and feeding difficulties. Other types include type 2 (intermediate SMA), type 3 (Kugelberg-Welander disease), and type 4 (adult-onset SMA).
The symptoms of SMA may include muscle wasting, fasciculations, weakness, hypotonia, respiratory difficulties, and mobility impairment. The diagnosis of SMA typically involves genetic testing to confirm the presence of a mutation in the SMN1 gene. Treatment options for SMA may include medications, physical therapy, assistive devices, and respiratory support.
The Survival Motor Neuron (SMN) complex is a protein complex that plays a crucial role in the biogenesis of small nuclear ribonucleoproteins (snRNPs), which are essential components of the spliceosome involved in pre-messenger RNA (pre-mRNA) splicing. The SMN complex consists of several proteins, including the SMN protein itself, Gemins2-8, and unrip.
The SMN protein is the central component of the complex and is encoded by the SMN1 gene located on chromosome 5q13.2. Mutations in this gene can lead to spinal muscular atrophy (SMA), a genetic disorder characterized by degeneration of motor neurons in the spinal cord, leading to muscle weakness and atrophy.
The SMN complex assembles in the cytoplasm and facilitates the assembly of spliceosomal snRNPs by helping to load Sm proteins onto small nuclear RNA (snRNA) molecules. Proper functioning of the SMN complex is essential for the correct splicing of pre-mRNA, and its dysfunction can lead to various developmental abnormalities and diseases, including SMA.
Survival of Motor Neuron 1 (SMN1) protein is a critical component for the survival of motor neurons, which are nerve cells that control muscle movements. The SMN1 protein is produced by the Survival of Motor Neuron 1 gene, located on human chromosome 5q13.
The primary function of the SMN1 protein is to assist in the biogenesis of small nuclear ribonucleoproteins (snRNPs), which are essential for spliceosomes - complex molecular machines responsible for RNA processing in the cell. The absence or significant reduction of SMN1 protein leads to defective snRNP assembly, impaired RNA splicing, and ultimately results in motor neuron degeneration.
Mutations in the SMN1 gene can cause Spinal Muscular Atrophy (SMA), a genetic disorder characterized by progressive muscle weakness, atrophy, and paralysis due to the loss of lower motor neurons in the spinal cord. The severity of SMA depends on the amount of functional SMN1 protein produced, with less protein leading to more severe symptoms.
Nerve tissue proteins are specialized proteins found in the nervous system that provide structural and functional support to nerve cells, also known as neurons. These proteins include:
1. Neurofilaments: These are type IV intermediate filaments that provide structural support to neurons and help maintain their shape and size. They are composed of three subunits - NFL (light), NFM (medium), and NFH (heavy).
2. Neuronal Cytoskeletal Proteins: These include tubulins, actins, and spectrins that provide structural support to the neuronal cytoskeleton and help maintain its integrity.
3. Neurotransmitter Receptors: These are specialized proteins located on the postsynaptic membrane of neurons that bind neurotransmitters released by presynaptic neurons, triggering a response in the target cell.
4. Ion Channels: These are transmembrane proteins that regulate the flow of ions across the neuronal membrane and play a crucial role in generating and transmitting electrical signals in neurons.
5. Signaling Proteins: These include enzymes, receptors, and adaptor proteins that mediate intracellular signaling pathways involved in neuronal development, differentiation, survival, and death.
6. Adhesion Proteins: These are cell surface proteins that mediate cell-cell and cell-matrix interactions, playing a crucial role in the formation and maintenance of neural circuits.
7. Extracellular Matrix Proteins: These include proteoglycans, laminins, and collagens that provide structural support to nerve tissue and regulate neuronal migration, differentiation, and survival.
Gene deletion is a type of mutation where a segment of DNA, containing one or more genes, is permanently lost or removed from a chromosome. This can occur due to various genetic mechanisms such as homologous recombination, non-homologous end joining, or other types of genomic rearrangements.
The deletion of a gene can have varying effects on the organism, depending on the function of the deleted gene and its importance for normal physiological processes. If the deleted gene is essential for survival, the deletion may result in embryonic lethality or developmental abnormalities. However, if the gene is non-essential or has redundant functions, the deletion may not have any noticeable effects on the organism's phenotype.
Gene deletions can also be used as a tool in genetic research to study the function of specific genes and their role in various biological processes. For example, researchers may use gene deletion techniques to create genetically modified animal models to investigate the impact of gene deletion on disease progression or development.
CREB (Cyclic AMP Response Element-Binding Protein) is a transcription factor that plays a crucial role in regulating gene expression in response to various cellular signals. CREB binds to the cAMP response element (CRE) sequence in the promoter region of target genes and regulates their transcription.
When activated, CREB undergoes phosphorylation at a specific serine residue (Ser-133), which leads to its binding to the coactivator protein CBP/p300 and recruitment of additional transcriptional machinery to the promoter region. This results in the activation of target gene transcription.
CREB is involved in various cellular processes, including metabolism, differentiation, survival, and memory formation. Dysregulation of CREB has been implicated in several diseases, such as cancer, neurodegenerative disorders, and mood disorders.
Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).
Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.
CASP8 and FADD-Like Apoptosis Regulating Protein, also known as CFLAR or FLIP, is a protein that plays a role in regulating cell death (apoptosis). It is a member of the inhibitor of apoptosis protein (IAP) family. The protein contains a death effector domain (DED), which allows it to interact with other proteins that contain DEDs, such as FADD and caspase-8.
CFLAR can function as an inhibitor or a promoter of apoptosis, depending on the context. When CFLAR is present in high levels, it can bind to and inhibit the activity of caspase-8, preventing the initiation of the apoptotic signaling pathway. However, when CFLAR is present in low levels or is cleaved by proteases, it can promote apoptosis by facilitating the activation of caspase-8.
Mutations in the gene that encodes CFLAR have been associated with an increased risk of developing certain types of cancer, such as Hodgkin lymphoma and diffuse large B-cell lymphoma.
Caspase-3 is a type of protease enzyme that plays a central role in the execution-phase of cell apoptosis, or programmed cell death. It's also known as CPP32 (CPP for ced-3 protease precursor) or apopain. Caspase-3 is produced as an inactive protein that is activated when cleaved by other caspases during the early stages of apoptosis. Once activated, it cleaves a variety of cellular proteins, including structural proteins, enzymes, and signal transduction proteins, leading to the characteristic morphological and biochemical changes associated with apoptotic cell death. Caspase-3 is often referred to as the "death protease" because of its crucial role in executing the cell death program.
Caspases are a family of protease enzymes that play essential roles in programmed cell death, also known as apoptosis. These enzymes are produced as inactive precursors and are activated when cells receive signals to undergo apoptosis. Once activated, caspases cleave specific protein substrates, leading to the characteristic morphological changes and DNA fragmentation associated with apoptotic cell death. Caspases also play roles in other cellular processes, including inflammation and differentiation. There are two types of caspases: initiator caspases (caspase-2, -8, -9, and -10) and effector caspases (caspase-3, -6, and -7). Initiator caspases are activated in response to various apoptotic signals and then activate the effector caspases, which carry out the proteolytic cleavage of cellular proteins. Dysregulation of caspase activity has been implicated in a variety of diseases, including neurodegenerative disorders, ischemic injury, and cancer.
Apoptosis regulatory proteins are a group of proteins that play an essential role in the regulation and execution of apoptosis, also known as programmed cell death. This process is a normal part of development and tissue homeostasis, allowing for the elimination of damaged or unnecessary cells. The balance between pro-apoptotic and anti-apoptotic proteins determines whether a cell will undergo apoptosis.
Pro-apoptotic proteins, such as BAX, BID, and PUMA, promote apoptosis by neutralizing or counteracting the effects of anti-apoptotic proteins or by directly activating the apoptotic pathway. These proteins can be activated in response to various stimuli, including DNA damage, oxidative stress, and activation of the death receptor pathway.
Anti-apoptotic proteins, such as BCL-2, BCL-XL, and MCL-1, inhibit apoptosis by binding and neutralizing pro-apoptotic proteins or by preventing the release of cytochrome c from the mitochondria, which is a key step in the intrinsic apoptotic pathway.
Dysregulation of apoptosis regulatory proteins has been implicated in various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Therefore, understanding the role of these proteins in apoptosis regulation is crucial for developing new therapeutic strategies to treat these conditions.
NAIP (gene)
Diablo homolog
XIAP
Caspase-9
Nerve tissue protein
Endogenous retrovirus
Hippocalcin
List of MeSH codes (D12.644)
Ted M. Dawson
NDR kinase
Low-affinity nerve growth factor receptor
SEMA3B
Excitatory synapse
List of MeSH codes (D12.776.476)
Soma (biology)
MAP3K12
14-Hydroxygelsenicine
DSCR1
KCNB1
Gonadotropin-inhibitory hormone
Protein kinase R
PAK2
Repulsive guidance molecule A
Valina L. Dawson
Autism spectrum
Programmed cell death
HIPK2
ID4
Rho family of GTPases
Semaphorin-3A
LINGO1
Human Neuronal apoptosis inhibitory protein (NAIP) ELISA Kit - Abbkine - Antibodies, proteins, biochemicals, assay kits for...
NAIP (gene) - Wikipedia
Spinal Muscular Atrophy: Background, Pathophysiology, Epidemiology
JCI - Parvalbumin interneuron loss mediates repeated anesthesia-induced memory deficits in mice
Kugelberg Welander Spinal Muscular Atrophy: Practice Essentials, Pathophysiology, Epidemiology
SMART: BIR domain annotation
DeCS
Human Viperin(Virus Inhibitory Protein) ELISA Kit - Orbital Biosciences online
NAIP Rabbit Polyclonal Antibody - Western Blot Antibodies - Bioworld Consulting Laboratories, LLC.
Neurol India: Table of Contents
Hippocalcin | Profiles RNS
Buffy
Changes in expression levels of Nod-like receptors in the spleen of ewes
Myelin Proteins | Harvard Catalyst Profiles | Harvard Catalyst
Frontiers | Sepsis-Induced Cardiomyopathy: Mechanisms and Treatments
Axon-soma communication in neuronal injury | Nature Reviews Neuroscience
Regulatory mechanisms of the anti-apoptotic NAIP gene during cellular stress and malignancy - Health Research BC
MeSH Browser
Pesquisa | Portal Regional da BVS
p75 neurotrophin receptor (p75NTR), FITC, Mouse Monoclonal Antibody
Ginsenoside Rg1 Protects against Oxidative Stress-induced Neuronal Apoptosis through Myosin IIA-actin Related Cytoskeletal...
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
The neuronal calcium sensor proteins GCAPs (guanylate cyclase activating proteins) switch - Apoptosis in amphibian organs
Neurogenic Disorders | Musculoskeletal Key
Biology | Free Full-Text | Sirtuin-3-Mediated Cellular Metabolism Links Cardiovascular Remodeling with Hypertension
IJMS | Free Full-Text | PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions
NAIP11
- This Human Neuronal apoptosis inhibitory protein (NAIP) ELISA Kit employs a two-site sandwich ELISA to quantitate NAIP in samples. (abbkine.com)
- Human Neuronal apoptosis inhibitory protein (NAIP) ELISA Kit has high sensitivity and excellent specificity for detection of Human NAIP. (abbkine.com)
- Neuronal apoptosis inhibitory protein encoded by NAIP contains regions of homology to two baculovirus inhibitor of apoptosis proteins, and it is able to suppress apoptosis induced by various signals. (abbkine.com)
- Baculoviral IAP repeat-containing protein 1 is a protein that in humans is encoded by the NAIP gene. (wikipedia.org)
- Expression of NLR family, including NOD1, NOD2, class II transactivator (CIITA), NLR family apoptosis inhibitory protein (NAIP), nucleotide-binding oligomerization domain, Leucine rich repeat and Pyrin domain containing 1 (NLRP1), NLRP3 and NLRP7, was analyzed using quantitative real-time PCR, Western blot and immunohistochemistry analysis. (animal-reproduction.org)
- In addition, expression values of NAIP and NLRP7 mRNA and proteins were improved at days 16 and 25 of pregnancy, and NLRP1 was peaked at days 13 and 16 of pregnancy in the maternal spleen. (animal-reproduction.org)
- Abadía-Molina F, Morón-Calvente V, Baird SD, Shamim F, Martín F, MacKenzie A. Neuronal apoptosis inhibitory protein (NAIP) localizes to the cytokinetic machinery during cell division. (animal-reproduction.org)
- Diez E, Yaraghi Z, MacKenzie A, Gros P. The neuronal apoptosis inhibitory protein (Naip) is expressed in macrophages and is modulated after phagocytosis and during intracellular infection with Legionella pneumophila . (animal-reproduction.org)
- Neuronal apoptosis inhibitory protein (NAIP) is particularly interesting because expression of NAIP is reported to be highly elevated in various leukemias. (healthresearchbc.ca)
- Two genes, i.e., survival motor neuron (SMN1) and neuronal apoptosis inhibitory protein (NAIP) are mapped to the SMA vicinity of chromosome 5q13. (bvsalud.org)
- Mutated proteins encoded by SMN1 and NAIP genes also result in degeneration and muscle weakness in SMA patients. (bvsalud.org)
Neurons11
- Each parvalbumin interneuron controls the activity of multiple pyramidal excitatory neurons, thereby regulating neuronal circuits and memory consolidation. (jci.org)
- Preventing the loss of parvalbumin neurons by deleting a proapoptotic protein, mitochondrial anchored protein ligase (MAPL), selectively in parvalbumin neurons rescued anesthesia-induced deficits in pyramidal cell inhibition and hippocampus-dependent long-term memory. (jci.org)
- A neuronal calcium-sensor protein that was initially found in the NEURONS of the HIPPOCAMPUS. (ouhsc.edu)
- The expression of human α-synuclein transgene in neuronal populations that include dopamine producing neurons under the control of Ddc -Gal4 produces a robust Parkinson disease model, and results in severely reduced lifespan and locomotor dysfunction. (sdbonline.org)
- A family of intracellular calcium-sensing proteins found predominately in NEURONS and PHOTORECEPTOR CELLS . (nih.gov)
- p75NTR is highly expressed in a number of non-neuronal and neuronal cells including motor neurons during development and also in damaged neurons. (biosensis.com)
- Oxidative stress-induced cytoskeletal dysfunction of neurons has been implicated as a crucial cause of cell apoptosis or death in the central nervous system (CNS) diseases, such as neurodegenerative and psychiatric diseases. (ijbs.com)
- The application of neuroprotectants rescuing the neurons from cytoskeletal damage and apoptosis can be a potential treatment for these CNS diseases. (ijbs.com)
- Meanwhile, both MH and Ac-DEVD-CHO had similar effects in protecting cell morphology, reducing LDH release, and inhibiting OGD-induced apoptosis in neurons. (syksignal.com)
- The majority of DEGs in excitatory and inhibitory neurons showed downregulation while most DEGs in oligodendrocytes, astrocytes, and microglia were upregulated. (hhv-6foundation.org)
- increase in mature neurons was unlikely due to suppressed apoptosis, because terminal deoxynucleotidyl transferase dUTP nick-end labeling analysis showed no difference in DNA terminal labeling between vehicle and 8-OH-DPAT-infused mice. (thetechnoant.info)
ELISA Kit2
- Porcine Leukemia Inhibitory Factor (LIF) ELISA Kit Introduction: The event of SARS-CoV-2 serological assessments is very large. (elisastrip.com)
- Description: Quantitativesandwich ELISA kit for measuring Human protein disulfide isomerase, PDI in samples from serum, plasma, tissue homogenates. (knoblauchpublishing.com)
Inhibitor3
- Domain found in inhibitor of apoptosis proteins (IAPs) and other proteins. (embl.de)
- It is found in proteins belonging to the IAP (inhibitor of apoptosis proteins) family. (embl.de)
- An inhibitor of apoptosis protein that was initially identified during analysis of CHROMOSOME DELETIONS associated with SPINAL MUSCULAR ATROPHY. (bvsalud.org)
Gene7
- An apoptosis-inhibiting gene from a nuclear polyhedrosis virus encoding a polypeptide with Cys/His sequence motifs. (embl.de)
- Using a genetic complementation assay to identify additional genes which inhibit apoptosis during infection with a p35 mutant, we have isolated a gene from Orgyia pseudotsugata NPV (OpMNPV) that was able to functionally substitute for AcMNPV p35. (embl.de)
- This study demonstrates that debcl and the pro-fission gene drp1 are necessary downstream of buffy to trigger a mitochondrial fragmentation during rbf1 -induced apoptosis. (sdbonline.org)
- Less is known regarding its critical role in neuronal physiology, neuronal metabolism, tissue homeostasis, and the control of gene expression in the central nervous system in healthy and diseased states. (mdpi.com)
- For example, using the 18-glycolsyl hydrolase protein Chi3L1 as a prototype, we were able to show that a single gene product can simultaneously suppress or promote injury and fibrosis depending on its temporospatial expression in the disease process. (yale.edu)
- The primary receptors from the Wnt proteins contain at least 10 family termed the Frizzled proteins following the 1st member, cells polarity gene I (Vinson et al. (ipa2014.org)
- Gene ontology functional enrichment analysis was performed using search tool for the retrieval of interacting genes/proteins. (ijpsonline.com)
Neurite outgrowth2
- It mediates signals of neurotrophins for neuronal survival, apoptosis, neurite outgrowth and synaptic plasticity. (biosensis.com)
- Under oxidative stress, the effects of maltol on cell viability, apoptosis, and neurite outgrowth were assessed. (molvis.org)
SMN11
- However, all patients with spinal muscular atrophy retain at least 1 copy of SMN2 , which generates only 10% of the amount of full-length SMN protein versus SMN1 . (medscape.com)
Inhibition3
- The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease . (sdbonline.org)
- After Foxc1 was overexpressed, the cognitive dysfunction of mice that underwent CLP surgery was improved, with the expression of IκBα also increased, microglial cell migration, the expression of p65, IL‑1β and TNF‑α and neuronal apoptosis were all decreased in vivo and in vitro , which were in turn reversed by the inhibition of IκBα in vitro . (spandidos-publications.com)
- 2014. Asparagus racemosus leaf extract inhibits growth of UOK 146 renal cell carcinoma cell line: simultaneous oncogenic PRCCTFE3 fusion transcript inhibition and apoptosis independent cell death. (raysahelian.com)
Hippocampus4
- Here, we show that repeated general anesthesia in postnatal mice induces preferential apoptosis and subsequent loss of parvalbumin-positive inhibitory interneurons in the hippocampus. (jci.org)
- The results showed impairment of hippocampus and striatal regions of brain after KA injection marked by an increase in lipid peroxidation and protein carbonyl content and decline in glutathione peroxidase (GPx) activity and reduced glutathione (GSH) content. (raysahelian.com)
- In view of such observations and arguments, we are prompted to focus on receptors and signaling molecules that are likely BCL2L to play crucial roles in sculpting the major neuronal centers such as the hippocampus in the neonatal brain. (thetechnoant.info)
- Thus, the G-protein-coupled 5-HT1A-R is present at significant levels in the P6 hippocampus to. (thetechnoant.info)
Inflammation6
- Lipopolysaccharide (LPS) treatment was found to trigger BV‑2 cell migration, inflammation and neuronal apoptosis. (spandidos-publications.com)
- Finally, in very recent work, we have collaborated with investigators in Yale's School of Immunobiology to describe a new innate immune process by which the inflammation associated hormone GDF15 (also called macrophage inhibitory cytokine 1) controls systemic inflammation and tissue responses via central regulation of peripheral tolerance in multiple organs. (yale.edu)
- The authors also described associations between cell subtypes and genes involved in inflammation, demyelination, protein folding and stability, neuronal and necrotic death, and T-cell activation and immunity, which pointed to cell-type specific responses to global cellular stress. (hhv-6foundation.org)
- ObjectiveTo study the inhibitory effect of Banxia Houputang (BHT) on lipopolysaccharide (LPS)-induced inflammation of microglia (BV2) cells and the neuroprotective effect on human neuroblastoma (SH-SY5Y) cells. (bvsalud.org)
- In addition, neuronal apoptosis model was established by co-culture of LPS-induced BV2 cell inflammation medium and SH-SY5Y cells (LPS-DMEM) and was administrated according to the above grouping. (bvsalud.org)
- Assessment of microglial activation in lesioned sites and protein markers for proinflammatory, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, interferon (IFN)-γ, and HMGB1 were used to evaluate neuroinflammatory responses and anti-inflammation effects of ω-3 PUFA supplementation. (biomedcentral.com)
Kinase6
- Interestingly, rbf1 -induced apoptosis leads to a debcl - and drp1 -dependent Reactive Oxygen Species production, which in turn activates the Jun Kinase pathway to trigger cell death. (sdbonline.org)
- The enzyme in question is c-jun-N-terminal kinase (JNK), pronounced 'junk,' which has been implicated in many processes in the body's response to stresses, such as oxidative stress , protein misfolding, and metabolic disorder. (medicalnewstoday.com)
- PKG: protein kinase G. (frontiersin.org)
- Crystallization and Structural Determination of ABLT315I:AP24534 The kinase domain of murine ABLT315I was coexpressed with YopH protein tyrosine phosphatase in E. coli as described previously and purified in the clear presence of AP24534 to near homogeneity using metal affinity, Mono Q, and measurement exclusion chroma tography. (smadpathway.com)
- Several downstream sign transduction pathways can mediate the natural response from the Wnt proteins including Dishevelled, -catenin, intracellular calcium mineral, proteins kinase C, Akt, and glycogen synthase kinase-3. (ipa2014.org)
- Equipped with a mouse model of stress (5-HT1A-R-/- mice) and a 5-HT1A-R-expressing hippocampal neuron-derived cell line, HN2-5, our earlier studies have reported that a 5-HT1A-R-mediated signaling pathway functions via extracellular receptor-activated kinase 1/2 (ERK1/2)-catalyzed activation of protein kinase C alpha (PKC) to promote synaptogenesis at P15 in the hippocampal CA1 region [12,16]. (thetechnoant.info)
Viability3
- The cell viability and apoptosis were determined by using adenosine 5′-triphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. (molvis.org)
- The lactic acid dehydrogenase (LDH) release rate, neuronal viability, and apoptotic rate were also detected. (syksignal.com)
- They also similarly improved neuronal viability after OGD. (syksignal.com)
Antibody4
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Virus Inhibitory Protein (Viperin) in tissue homogenates, cell lysates and other biological fluids. (orbitalbiosciences.com)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Virus Inhibitory Protein (Viperin) in samples from tissue homogenates, cell lysates and other biological fluids with no significant corss-reactivity with analogues from other species. (orbitalbiosciences.com)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Protein Disulfide Isomerase (PDI) in serum, plasma, tissue homogenates and other biological fluids. (knoblauchpublishing.com)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Protein Disulfide Isomerase (PDI) in samples from serum, plasma, tissue homogenates and other biological fluids with no significant corss-reactivity with analogues from other species. (knoblauchpublishing.com)
Anti-apoptotic2
- The critical motifs required for anti-apoptotic activity of IAP proteins are the BIRs. (embl.de)
- It has been previously shown that rbf1 pro-apoptotic activity depends on its ability to decrease the level of anti-apoptotic proteins such as the Bcl-2 family protein Buffy. (sdbonline.org)
Autophagy1
- Common upregulated genes shared across cell types in late-stage pathology were involved in protein folding and were associated with autophagy, apoptosis, and generalized stress response. (hhv-6foundation.org)
Mediates1
- p75NTR also acts as a co-receptor for NOGO which mediates inhibitory signals of myelin associated protein. (biosensis.com)
Oxidative3
- The current study is to reveal the regulatory effects of Rg1 on cytoskeletal and morphological lesion in oxidative stress-induced neuronal apoptosis. (ijbs.com)
- The results demonstrated that pre-treatment with Rg1 (0.1-10 μM) attenuated hydrogen peroxide (H 2 O 2 )-induced neuronal apoptosis and oxidative stress through reducing the intracellular reactive oxygen species (ROS) production and methane dicarboxylic aldehyde (MDA) level. (ijbs.com)
- RCAN1 is upregulated by stress factors, such as protein aggregates, elevated intracellular calcium, oxidative stress, and glucocorticoid, prevents excess and dangerous over-activation of calcineurin. (molcells.org)
Interacts1
- High-mobility group box 1 (HMGB1) protein, an important mediator in late inflammatory responses, interacts with transmembrane receptor for advanced glycation end products (RAGE) and toll-like receptors (TLRs) to activate downstream signaling pathways, such as the nuclear factor (NF)-κB signaling pathway, leading to a cascade amplification of inflammatory responses, which are related to neuronal damage after TBI. (biomedcentral.com)
Programmed cell3
- Apoptosis, or programmed cell death, is a critical physiological process that is turned on and off as appropriate to eliminate abnormal cells. (healthresearchbc.ca)
- The genetic mechanisms that inhibit activation of the apoptosis protein (IAP) family include molecules that sequester key enzymes necessary for turning on and sustaining the process of programmed cell death. (healthresearchbc.ca)
- That migration, coupled with JNK activation, is associated with a number of serious health issues, including apoptosis or programmed cell death, liver damage, neuronal cell death, stroke and heart attack. (medicalnewstoday.com)
Guanylate2
- The neuronal calcium sensor proteins GCAPs (guanylate cyclase activating proteins) switch between Ca2+-free and Ca2+-bound conformational states and confer calcium sensitivity to guanylate cyclase at retinal photoreceptor cells. (phytid.org)
- To assay whether the transgenic bEF?GCAP2 protein has the capacity to activate Ret-GC activity in retinal extracts from mice in a comparable manner as in studies we performed guanylate cyclase activity assays in retinal extracts from the mutant or control mice obtained prior to significant retinal degeneration -between p20 and p30 - under conditions of 0 Ca2+ or 2 M Ca2+ (Fig. 3). (phytid.org)
Pathways3
- The aim of the present work is to review cumulative evidence regarding the participation of PI3K pathways in neuronal function, focusing on their role in neuronal metabolism and transcriptional regulation of genes involved in neuronal maintenance and plasticity or on the expression of pathological hallmarks associated with neurodegeneration. (mdpi.com)
- In addition, a lot more than eighty focus on Monooctyl succinate genes of Wnt signaling pathways have already been confirmed in Monooctyl succinate individual also, mouse, which Monooctyl succinate has an 85-amino acidity domain close to the middle of proteins (Nusse and Varmus, 1992). (ipa2014.org)
- Many recent studies likewise have demonstrated that the various subsets of Wnt protein can donate to specific physiological adjustments through triggering different intracellular pathways (Heisenberg et al. (ipa2014.org)
Assay1
- Description: A sandwich quantitative ELISA assay kit for detection of Human Protein Disulfide Isomerase (PDI) in samples from serum, plasma, tissue homogenates or other biological fluids. (knoblauchpublishing.com)
Amino Acids1
- Immunogen Description Recombinant extracellular domain (amino acids 29-250) of human NGFR/p75NTR protein with N-terminal His-tag. (biosensis.com)
Membrane Proteins1
- Because of the difficulties of generating conformational mAbs against complex and highly conserved membrane proteins, no reliable tools exist to measure GLUT4 at the cell surface, follow its trafficking, or detect the conformational state of the protein. (pubchase.com)
Inhibitors3
Induces1
- The Drosophila retinoblastoma protein, Rbf1, induces a debcl and drp1 -dependent mitochondrial apoptosis. (sdbonline.org)
Intracellular calcium2
- Neuronal calcium-sensor proteins interact with other regulatory proteins to mediate physiological responses to a change in intracellular calcium concentration. (nih.gov)
- These Wnt protein bind the transmembrane receptor to activate heterotrimeric G protein and boost intracellular calcium amounts. (ipa2014.org)
Baculovirus1
- The 'baculovirus inhibitior of apoptosis protein repeat' (BIR) [ ( PUBMED:8139034 ) ( PUBMED:8552191 ) ] is a domain of about 70 residues arranged in tandem repeats separated by a variable length linker, that seems to confer cell death-preventing activity. (embl.de)
Neurological2
- Many studies have found that MH improves the neurological function of patients with HIE by reducing neuronal apoptosis [7,8]. (syksignal.com)
- It was found that ω-3 PUFA supplementation inhibited TBI-induced microglial activation and expression of inflammatory factors (TNF-α, IL-1β, IL-6, and IFN-γ), reduced brain edema, decreased neuronal apoptosis, and improved neurological functions after TBI. (biomedcentral.com)
Synaptic1
- FEAST: A flow cytometry-based toolkit for interrogating microglial engulfment of synaptic and myelin proteins. (harvard.edu)
Myelin5
- Myelin Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
- Proteins found in the myelin sheath. (harvard.edu)
- This graph shows the total number of publications written about "Myelin Proteins" by people in Harvard Catalyst Profiles by year, and whether "Myelin Proteins" was a major or minor topic of these publication. (harvard.edu)
- Below are the most recent publications written about "Myelin Proteins" by people in Profiles. (harvard.edu)
- Protein citrullination marks myelin protein aggregation and disease progression in mouse ALS models. (harvard.edu)
Family4
- Buffy often acts opposite to Debcl , the other Drosophila Bcl-2-family protein. (sdbonline.org)
- These results provide a mechanism by which Drosophila Bcl-2 family proteins can control apoptosis and shed light on a link between Rbf1 and mitochondrial dynamics, in vivo. (sdbonline.org)
- Pannexin-1 (PANX1) is an approximately 45 kDa member of the Pannexin family of four-transmembrane channel proteins with a conserved pattern of cysteines. (rndsystems.com)
- A family of homologous proteins of low MOLECULAR WEIGHT that are predominately expressed in the BRAIN and that have been implicated in a variety of human diseases. (nih.gov)
Ligand1
- Single-chain formats of TNF-related apoptosis inducing ligand (scTRAIL) can serve as effector components of tumour-associated antigen-targeted as well as non-targeted fusion proteins, being characterized by high tumour cell-specific induction of apoptosis through death receptor activation. (pubchase.com)
Tumour3
- IgG-single-chain TRAIL fusion proteins for tumour therapy. (pubchase.com)
- The binding specificity to EGFR and death receptors was retained in all IgG-scTRAIL formats and translated into high antigen-specific bioactivity on EGFR-positive Colo205, HCT116 and WM1366 tumour cell lines, with or without sensitization to apoptosis by bortezomib. (pubchase.com)
- As prooxidants, polyphenols may stimulate apoptosis and inhibit tumour growth [ 8 ]. (hindawi.com)
Mitochondrial2
- Notably, Debcl modulates Drp1 mitochondrial localization during apoptosis. (sdbonline.org)
- Mitochondrial porin , also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. (sdbonline.org)
Peptides1
- We found that only IGLC1 the distinct isoforms of 14-3-3 proteins fulfilled these criteria, being identified with a considerably higher number of peptides [1.33 to 3.2-fold higher] in the GCAPs? (phytid.org)
Signals1
- Apoptosis is a highly regulated process receiving many activating and inhibiting signals, but the final outcome relies on which signals tip the scale. (healthresearchbc.ca)
Microglial3
- In the present study, the mechanistic role of Foxc1 on microglial migration, neuroinflammation and neuronal apoptosis during the occurrence of cognitive dysfunction in SAE was investigated. (spandidos-publications.com)
- Overall, these results suggest that the overexpression of Foxc1 inhibited microglial migration whilst suppressing the inflammatory response and neuronal apoptosis by regulating the IκBα/NF‑κB pathway, thereby improving cognitive dysfunction during SAE. (spandidos-publications.com)
- TBI-induced microglial activation and the release of inflammatory factors, such as tumor necrosis factor (TNF), interleukin (IL), and interferon (IFN), cause direct neuronal cell death and also induce vascular endothelial cells to express a variety of cell adhesion molecules and cell chemotaxis. (biomedcentral.com)
Protects1
- In conclusion, caspase-3 serves as a key intervention point of the key modulation site or regulatory region in MH treatment that protects neuronal apoptosis against OGD injury. (syksignal.com)
Cell morphology1
- In the C57MG mouse, transient manifestation of Wnt1, Wnt2 and Wnt3a in mammary epithelial cells could cause morphological change while the additional Wnt proteins possess little influence on cell morphology (Wong et al. (ipa2014.org)
Damage2
- When the antioxidant system is overloaded, ROS will damage proteins, DNA, and lipids [ 4 ]. (hindawi.com)
- We designed this study to investigate the potential of extract of Asparagus racemosus against kainic acid (KA)-induced hippocampal and striatal neuronal damage. (raysahelian.com)
Caspase2
- Its conductance is increased in response to hypoxia, isotonic stress, NMDA R activation, and Caspase-3 and -7 activation during apopotosis. (rndsystems.com)
- Apoptosis is the result of a biochemical cascade and caspase pro- teases are major participants in the apoptotic program [9]. (syksignal.com)
Cardiac1
- 1993). Desk 1 Neuronal and cardiac manifestation from the Wnt as well as the Wnt receptor with natural function. (ipa2014.org)
Therapeutic1
- Understanding the proteins that regulate the 5-HT1A promoter will lead to insights on receptor regulation and provide new therapeutic targets relevant to depression, anxiety, obsessive compulsive disorder and other mental illnesses. (vdocuments.net)
Dysfunction1
- We first identified the bioactive phytoconstituents from Amaranthus tricolor and predicted their potential protein targets involved in the pathogenesis of cognitive dysfunction using BindingDB (p≥0.7). (ijpsonline.com)
Mechanisms1
- The extensive lengths of neuronal processes necessitate efficient mechanisms for communication with the cell body. (nature.com)
Regulatory1
- The CPC includes, as well as Aurora B, three regulatory subunits: the inner centromeric protein, Survivin, and Borealin/Dasra W. Beginning in prophase, the CPC localizes to condensing chromosomes and steadily concentrates at the internal centromere where one function would be to correct poor Infectious causes of cancer spindle kinetochore devices. (smadpathway.com)
Biological1
- Intrinsic brain RAS is an enzyme-neuropeptide system having functional components (angiotensinogen, peptidases, angiotensin, and specific receptor proteins) with important biological and neurobiological activities in the brain. (hindawi.com)
Processes2
- More recent work focuses on how neuronal guidance proteins are involved in these processes, and in modeling the biophysical attributes of the normal and diseased adult lung. (yale.edu)
- In delineating the processes described above, we discovered an unexpected contribution of neuronal guidance proteins (NGPs) to IPF and related diseases. (yale.edu)
Cells2
- Expression of circular RNA CDR1-AS in colon cancer cells increases cell surface PD-L1 protein levels. (harvard.edu)
- Many people of Wnt protein have been determined to regulate proliferation, differentiation, and loss of life of varied cells. (ipa2014.org)