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Search results 901 to 968 out of 968 for Tub

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0.088s
Type Details Score
Protein
Organism: Mus musculus/domesticus
Length: 505  
Fragment?: false
Publication
First Author: Rybiczka-Tešulov M
Year: 2024
Journal: Nat Commun
Title: Circular RNAs regulate neuron size and migration of midbrain dopamine neurons during development.
Volume: 15
Issue: 1
Pages: 6773
Protein
Organism: Mus musculus/domesticus
Length: 543  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 122  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 219  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 457  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 108  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 457  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 492  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 256  
Fragment?: true
Publication
First Author: Carroll K
Year: 2004
Journal: Nat Rev Mol Cell Biol
Title: Tubby proteins: the plot thickens.
Volume: 5
Issue: 1
Pages: 55-63
Protein
Organism: Mus musculus/domesticus
Length: 156  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 274  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 232  
Fragment?: false
Protein Domain
Type: Domain
Description: Tubby, an autosomal recessive mutation, mapping to mouse chromosome 7, was recently found to be the result of a splicing defect in a novel gene with unknown function. This mutation maps to the tub gene [, ]. The mouse tubby mutation is the cause of maturity-onset obesity, insulin resistance and sensory deficits. By contrast with the rapid juvenile-onset weight gain seen in diabetes (db) and obese (ob) mice, obesity in tubby mice develops gradually, and strongly resembles the late-onset obesity observed in the human population. Excessive deposition of adipose tissue culminates in a two-fold increase of body weight. Tubby mice also suffer retinal degeneration and neurosensory hearing loss. The tripartite character of the tubby phenotype is highly similar to human obesity syndromes, such as Alstrom and Bardet-Biedl. Although these phenotypes indicate a vital role for tubby proteins, no biochemical function has yet been ascribed to any family member [], although it has been suggested that the phenotypic features of tubby mice may be the result of cellular apoptosis triggered by expression of the mutated tub gene. TUB is the founding-member of the tubby-like proteins, the TULPs. TULPs are found in multicellular organisms from both the plant and animal kingdoms. Ablation of members of this protein family cause disease phenotypes that are indicative of their importance in nervous-system function and development [].Mammalian TUB is a hydrophilic protein of ~500 residues. The N-terminal () portion of the protein is conserved neither in length nor sequence, but, in TUB, contains the nuclear localisation signal and may have transcriptional-activation activity. The C-terminal 250 residues are highly conserved. The C-terminal extremity contains a cysteine residue that might play an important role in the normal functioning of these proteins. The crystal structure of the C-terminal core domain from mouse tubby has been determined to 1.9A resolution. This domain is arranged as a 12-stranded, all anti-parallel, closed β-barrel that surrounds a central alpha helix, (which is at the extreme carboxyl terminus of the protein) that forms most of the hydrophobic core. Structural analyses suggest that TULPs constitute a unique family of bipartite transcription factors [].
Protein Domain
Type: Homologous_superfamily
Description: Tubby, an autosomal recessive mutation, mapping to mouse chromosome 7, was recently found to be the result of a splicing defect in a novel gene with unknown function. This mutation maps to the tub gene [, ]. The mouse tubby mutation is the cause of maturity-onset obesity, insulin resistance and sensory deficits. By contrast with the rapid juvenile-onset weight gain seen in diabetes (db) and obese (ob) mice, obesity in tubby mice develops gradually, and strongly resembles the late-onset obesity observed in the human population. Excessive deposition of adipose tissue culminates in a two-fold increase of body weight. Tubby mice also suffer retinal degeneration and neurosensory hearing loss. The tripartite character of the tubby phenotype is highly similar to human obesity syndromes, such as Alstrom and Bardet-Biedl. Although these phenotypes indicate a vital role for tubby proteins, no biochemical function has yet been ascribed to any family member [], although it has been suggested that the phenotypic features of tubby mice may be the result of cellular apoptosis triggered by expression of the mutated tub gene. TUB is the founding-member of the tubby-like proteins, the TULPs. TULPs are found in multicellular organisms from both the plant and animal kingdoms. Ablation of members of this protein family cause disease phenotypes that are indicative of their importance in nervous-system function and development [].Mammalian TUB is a hydrophilic protein of ~500 residues. The N-terminal () portion of the protein is conserved neither in length nor sequence, but, in TUB, contains the nuclear localisation signal and may have transcriptional-activation activity. The C-terminal 250 residues are highly conserved. The C-terminal extremity contains a cysteine residue that might play an important role in the normal functioning of these proteins. The crystal structure of the C-terminal core domain from mouse tubby has been determined to 1.9A resolution. This domain is arranged as a 12-stranded, all anti-parallel, closed β-barrel that surrounds a central alpha helix, (which is at the extreme carboxyl terminus of the protein) that forms most of the hydrophobic core. Structural analyses suggest that TULPs constitute a unique family of bipartite transcription factors [].This superfamily represents the tubby C-terminal domain and the structurally related LURP1-like domain.
Protein Domain
Type: Conserved_site
Description: Tubby, an autosomal recessive mutation, mapping to mouse chromosome 7, was recently found to be the result of a splicing defect in a novel gene with unknown function. This mutation maps to the tub gene [, ]. The mouse tubby mutation is the cause of maturity-onset obesity, insulin resistance and sensory deficits. By contrast with the rapid juvenile-onset weight gain seen in diabetes (db) and obese (ob) mice, obesity in tubby mice develops gradually, and strongly resembles the late-onset obesity observed in the human population. Excessive deposition of adipose tissue culminates in a two-fold increase of body weight. Tubby mice also suffer retinal degeneration and neurosensory hearing loss. The tripartite character of the tubby phenotype is highly similar to human obesity syndromes, such as Alstrom and Bardet-Biedl. Although these phenotypes indicate a vital role for tubby proteins, no biochemical function has yet been ascribed to any family member [], although it has been suggested that the phenotypic features of tubby mice may be the result of cellular apoptosis triggered by expression of the mutated tub gene. TUB is the founding-member of the tubby-like proteins, the TULPs. TULPs are found in multicellular organisms from both the plant and animal kingdoms. Ablation of members of this protein family cause disease phenotypes that are indicative of their importance in nervous-system function and development [].Mammalian TUB is a hydrophilic protein of ~500 residues. The N-terminal () portion of the protein is conserved neither in length nor sequence, but, in TUB, contains the nuclear localisation signal and may have transcriptional-activation activity. The C-terminal 250 residues are highly conserved. The C-terminal extremity contains a cysteine residue that might play an important role in the normal functioning of these proteins. The crystal structure of the C-terminal core domain from mouse tubby has been determined to 1.9A resolution. This domain is arranged as a 12-stranded, all anti-parallel, closed β-barrel that surrounds a central alpha helix, (which is at the extreme carboxyl terminus of the protein) that forms most of the hydrophobic core. Structural analyses suggest that TULPs constitute a unique family of bipartite transcription factors [].This entry represents conserved sites found in the C-terminal domain. The site closest to the C terminus contains a penultimate cysteine residue that could be critical to the normal functioning of these proteins.
Genotype
Symbol: Tulp3/Tulp3 Pkd1/Pkd1<+> Tg(Pax8-rtTA2S*M2)1Koes/? Tg(tetO-cre)1Jaw/?
Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA * SJL
Zygosity: cn
Has Mutant Allele: true
Genotype
Symbol: Tulp3/Tulp3<+> Pkd1/Pkd1 Tg(Pax8-rtTA2S*M2)1Koes/? Tg(tetO-cre)1Jaw/?
Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA * SJL
Zygosity: cn
Has Mutant Allele: true
Protein
Organism: Mus musculus/domesticus
Length: 42  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 673  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 144  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 486  
Fragment?: false
Publication  
First Author: Constable S
Year: 2020
Journal: Development
Title: The ciliary phosphatidylinositol phosphatase Inpp5e plays positive and negative regulatory roles in Shh signaling.
Volume: 147
Issue: 3
Publication  
First Author: Zhao Y
Year: 2018
Journal: Exp Eye Res
Title: A comprehensive spatial-temporal transcriptomic analysis of differentiating nascent mouse lens epithelial and fiber cells.
Volume: 175
Pages: 56-72
Protein
Organism: Mus musculus/domesticus
Length: 1354  
Fragment?: false
Publication
First Author: Hayashi S
Year: 2016
Journal: PLoS Genet
Title: Gata6-Dependent GLI3 Repressor Function is Essential in Anterior Limb Progenitor Cells for Proper Limb Development.
Volume: 12
Issue: 6
Pages: e1006138
Publication
First Author: Augustin M
Year: 2005
Journal: Mamm Genome
Title: Efficient and fast targeted production of murine models based on ENU mutagenesis.
Volume: 16
Issue: 6
Pages: 405-13
Protein
Organism: Mus musculus/domesticus
Length: 1547  
Fragment?: false
Publication
First Author: Nagle DL
Year: 1999
Journal: Nature
Title: The mahogany protein is a receptor involved in suppression of obesity.
Volume: 398
Issue: 6723
Pages: 148-52
Publication
First Author: York B
Year: 1996
Journal: Mamm Genome
Title: Sensitivity to dietary obesity linked to a locus on chromosome 15 in a CAST/Ei x C57BL/6J F2 intercross.
Volume: 7
Issue: 9
Pages: 677-81
Publication
First Author: Samuelson LC
Year: 1995
Journal: Mamm Genome
Title: Localization of the murine cholecystokinin A and B receptor genes.
Volume: 6
Issue: 4
Pages: 242-6
Publication
First Author: Kalinichenko VV
Year: 1999
Journal: J Immunol
Title: Norepinephrine-mediated inhibition of antitumor cytotoxic T lymphocyte generation involves a beta-adrenergic receptor mechanism and decreased TNF-alpha gene expression.
Volume: 163
Issue: 5
Pages: 2492-9
Publication
First Author: Qin J
Year: 2011
Journal: Proc Natl Acad Sci U S A
Title: Intraflagellar transport protein 122 antagonizes Sonic Hedgehog signaling and controls ciliary localization of pathway components.
Volume: 108
Issue: 4
Pages: 1456-61
Publication      
First Author: The UK Mouse Genome Centre European Consortium
Year: 2000
Journal: Database Release
Title: European Consortium EST Radiation Hybrid Database
Publication
First Author: Klattig J
Year: 2007
Journal: Sex Dev
Title: WT1-mediated gene regulation in early urogenital ridge development.
Volume: 1
Issue: 4
Pages: 238-54
Publication
First Author: Gurdziel K
Year: 2016
Journal: Dev Dyn
Title: Transcriptome of the inner circular smooth muscle of the developing mouse intestine: Evidence for regulation of visceral smooth muscle genes by the hedgehog target gene, cJun.
Volume: 245
Issue: 5
Pages: 614-26
Publication      
First Author: NIH Mouse Knockout Inventory
Year: 2004
Journal: MGI Direct Data Submission
Title: Information obtained from the NIH Mouse Knockout Inventory
Publication      
First Author: MGI and IMPC
Year: 2017
Journal: MGI Direct Data Submission
Title: MGI Curation of Endonuclease-Mediated Alleles (CRISPR) from the International Mouse Phenotyping Consortium (IMPC)
Publication
First Author: Dickinson ME
Year: 2016
Journal: Nature
Title: High-throughput discovery of novel developmental phenotypes.
Volume: 537
Issue: 7621
Pages: 508-514
Publication      
First Author: The Jackson Laboratory Backcross DNA Panel Mapping Resource
Year: 1999
Journal: Database Release
Title: JAX BSS Panel Mapping Data
Publication        
First Author: UniProt-GOA
Year: 2012
Title: Gene Ontology annotation based on UniPathway vocabulary mapping
Publication
First Author: Friedel RH
Year: 2007
Journal: Brief Funct Genomic Proteomic
Title: EUCOMM--the European conditional mouse mutagenesis program.
Volume: 6
Issue: 3
Pages: 180-5
Publication      
First Author: International Knockout Mouse Consortium
Year: 2014
Journal: Database Download
Title: MGI download of modified allele data from IKMC and creation of new knockout alleles
Publication      
First Author: MGI and IMPC
Year: 2018
Journal: Database Release
Title: MGI Load of Endonuclease-Mediated Alleles (CRISPR) from the International Mouse Phenotyping Consortium (IMPC)
Publication        
First Author: Mouse Genome Informatics Scientific Curators
Year: 2001
Title: RIKEN Data Curation in Mouse Genome Informatics
Publication      
First Author: Wellcome Trust Sanger Institute
Year: 2010
Journal: MGI Direct Data Submission
Title: Alleles produced for the EUCOMM and EUCOMMTools projects by the Wellcome Trust Sanger Institute
Publication      
First Author: International Mouse Strain Resource
Year: 2014
Journal: Database Download
Title: MGI download of germline transmission data for alleles from IMSR strain data
Publication        
First Author: Mouse Genome Informatics Scientific Curators
Year: 2003
Title: Data Curation Using Mouse Genome Assembly
Publication      
First Author: Shanghai Model Organisms Center
Year: 2017
Journal: MGI Direct Data Submission
Title: Information obtained from the Shanghai Model Organisms Center (SMOC), Shanghai, China
Publication      
First Author: Wellcome Trust Sanger Institute
Year: 2009
Journal: MGI Direct Data Submission
Title: Alleles produced for the KOMP project by the Wellcome Trust Sanger Institute
Publication      
First Author: Mouse Genome Informatics and the International Mouse Phenotyping Consortium (IMPC)
Year: 2014
Journal: Database Release
Title: Obtaining and Loading Phenotype Annotations from the International Mouse Phenotyping Consortium (IMPC) Database
Publication
First Author: Adams DJ
Year: 2024
Journal: Nature
Title: Genetic determinants of micronucleus formation in vivo.
Volume: 627
Issue: 8002
Pages: 130-136
Publication  
First Author: Bedogni F
Year: 2021
Journal: Front Mol Neurosci
Title: Cell-Type-Specific Gene Expression in Developing Mouse Neocortex: Intermediate Progenitors Implicated in Axon Development.
Volume: 14
Pages: 686034
Publication
First Author: Koscielny G
Year: 2014
Journal: Nucleic Acids Res
Title: The International Mouse Phenotyping Consortium Web Portal, a unified point of access for knockout mice and related phenotyping data.
Volume: 42
Issue: Database issue
Pages: D802-9
Publication      
First Author: Lennon G
Year: 1999
Journal: Database Download
Title: WashU-HHMI Mouse EST Project
Publication
First Author: Skarnes WC
Year: 2011
Journal: Nature
Title: A conditional knockout resource for the genome-wide study of mouse gene function.
Volume: 474
Issue: 7351
Pages: 337-42
Publication
First Author: Hansen GM
Year: 2008
Journal: Genome Res
Title: Large-scale gene trapping in C57BL/6N mouse embryonic stem cells.
Volume: 18
Issue: 10
Pages: 1670-9
Publication      
First Author: GUDMAP Consortium
Year: 2004
Journal: www.gudmap.org
Title: GUDMAP: the GenitoUrinary Development Molecular Anatomy Project
Publication
First Author: Gerhard DS
Year: 2004
Journal: Genome Res
Title: The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).
Volume: 14
Issue: 10B
Pages: 2121-7
Publication
First Author: Zambrowicz BP
Year: 2003
Journal: Proc Natl Acad Sci U S A
Title: Wnk1 kinase deficiency lowers blood pressure in mice: a gene-trap screen to identify potential targets for therapeutic intervention.
Volume: 100
Issue: 24
Pages: 14109-14
Publication        
First Author: GOA curators
Year: 2016
Title: Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Publication      
First Author: Mouse Genome Informatics (MGI) and National Center for Biotechnology Information (NCBI)
Year: 2008
Journal: Database Download
Title: Mouse Gene Trap Data Load from dbGSS
Publication
First Author: Okazaki Y
Year: 2002
Journal: Nature
Title: Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.
Volume: 420
Issue: 6915
Pages: 563-73
Publication
First Author: Kawai J
Year: 2001
Journal: Nature
Title: Functional annotation of a full-length mouse cDNA collection.
Volume: 409
Issue: 6821
Pages: 685-90
Publication        
First Author: MGD Nomenclature Committee
Year: 1995
Title: Nomenclature Committee Use
Publication
First Author: Diez-Roux G
Year: 2011
Journal: PLoS Biol
Title: A high-resolution anatomical atlas of the transcriptome in the mouse embryo.
Volume: 9
Issue: 1
Pages: e1000582
Publication      
First Author: MGI Genome Annotation Group and UniGene Staff
Year: 2015
Journal: Database Download
Title: MGI-UniGene Interconnection Effort