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Search results 3801 to 3900 out of 12470 for Impact

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Type Details Score
Publication
First Author: Zhang L
Year: 2024
Journal: Commun Biol
Title: Glutamate oxaloacetate transaminase 1 is dispensable in macrophage differentiation and anti-pathogen response.
Volume: 7
Issue: 1
Pages: 817
Publication
First Author: Martinez-Terroba E
Year: 2024
Journal: Sci Immunol
Title: Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment.
Volume: 9
Issue: 96
Pages: eadh5462
Publication
First Author: Reizel Y
Year: 2015
Journal: Genes Dev
Title: Gender-specific postnatal demethylation and establishment of epigenetic memory.
Volume: 29
Issue: 9
Pages: 923-33
Publication  
First Author: Samara C
Year: 2013
Journal: Front Cell Neurosci
Title: Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions.
Volume: 7
Pages: 228
Publication
First Author: Ray S
Year: 2015
Journal: G3 (Bethesda)
Title: An Examination of Dynamic Gene Expression Changes in the Mouse Brain During Pregnancy and the Postpartum Period.
Volume: 6
Issue: 1
Pages: 221-33
Publication
First Author: Lavin Y
Year: 2014
Journal: Cell
Title: Tissue-resident macrophage enhancer landscapes are shaped by the local microenvironment.
Volume: 159
Issue: 6
Pages: 1312-26
Publication
First Author: M Real F
Year: 2020
Journal: Science
Title: The mole genome reveals regulatory rearrangements associated with adaptive intersexuality.
Volume: 370
Issue: 6513
Pages: 208-214
Publication
First Author: Sun L
Year: 2013
Journal: Proc Natl Acad Sci U S A
Title: Long noncoding RNAs regulate adipogenesis.
Volume: 110
Issue: 9
Pages: 3387-92
Publication
First Author: Bonthuis PJ
Year: 2015
Journal: Cell Rep
Title: Noncanonical Genomic Imprinting Effects in Offspring.
Volume: 12
Issue: 6
Pages: 979-91
Publication
First Author: Shi X
Year: 2024
Journal: Sci Adv
Title: Compromised macrophages contribute to progression of MASH to hepatocellular carcinoma in FGF21KO mice.
Volume: 10
Issue: 43
Pages: eado9311
Publication  
First Author: Binns MM
Year: 1985
Journal: J Gen Virol
Title: Cloning and sequencing of the gene encoding the spike protein of the coronavirus IBV.
Volume: 66 ( Pt 4)
Pages: 719-26
Publication
First Author: Godeke GJ
Year: 2000
Journal: J Virol
Title: Assembly of spikes into coronavirus particles is mediated by the carboxy-terminal domain of the spike protein.
Volume: 74
Issue: 3
Pages: 1566-71
Publication
First Author: Chang KW
Year: 2000
Journal: Virology
Title: Coronavirus-induced membrane fusion requires the cysteine-rich domain in the spike protein.
Volume: 269
Issue: 1
Pages: 212-24
Publication
First Author: Belouzard S
Year: 2009
Journal: Proc Natl Acad Sci U S A
Title: Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites.
Volume: 106
Issue: 14
Pages: 5871-6
Publication
First Author: Lu G
Year: 2015
Journal: Trends Microbiol
Title: Bat-to-human: spike features determining 'host jump' of coronaviruses SARS-CoV, MERS-CoV, and beyond.
Volume: 23
Issue: 8
Pages: 468-78
Publication
First Author: Schwartz C
Year: 2019
Journal: Allergy
Title: Spontaneous atopic dermatitis in mice with a defective skin barrier is independent of ILC2 and mediated by IL-1β.
Volume: 74
Issue: 10
Pages: 1920-1933
Publication
First Author: Zhou W
Year: 2022
Journal: Nature
Title: ZBTB46 defines and regulates ILC3s that protect the intestine.
Volume: 609
Issue: 7925
Pages: 159-165
Publication
First Author: Godinho-Silva C
Year: 2019
Journal: Nature
Title: Light-entrained and brain-tuned circadian circuits regulate ILC3s and gut homeostasis.
Volume: 574
Issue: 7777
Pages: 254-258
Publication
First Author: Papaioannou NE
Year: 2021
Journal: Nat Commun
Title: Environmental signals rather than layered ontogeny imprint the function of type 2 conventional dendritic cells in young and adult mice.
Volume: 12
Issue: 1
Pages: 464
Publication
First Author: Pierson W
Year: 2013
Journal: Nat Immunol
Title: Antiapoptotic Mcl-1 is critical for the survival and niche-filling capacity of Foxp3⁺ regulatory T cells.
Volume: 14
Issue: 9
Pages: 959-65
Publication
First Author: Kuno A
Year: 2022
Journal: PLoS Biol
Title: DAJIN enables multiplex genotyping to simultaneously validate intended and unintended target genome editing outcomes.
Volume: 20
Issue: 1
Pages: e3001507
Protein
Organism: Mus musculus/domesticus
Length: 2201  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 2126  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 2126  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 2151  
Fragment?: false
Publication
First Author: Zhang W
Year: 2018
Journal: Biochem Biophys Res Commun
Title: Structural characterization of the HCoV-229E fusion core.
Volume: 497
Issue: 2
Pages: 705-712
Publication
First Author: Yan L
Year: 2018
Journal: Acta Crystallogr D Struct Biol
Title: Crystal structure of the post-fusion core of the Human coronavirus 229E spike protein at 1.86 Å resolution.
Volume: 74
Issue: Pt 9
Pages: 841-851
Protein
Organism: Mus musculus/domesticus
Length: 304  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 110  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 109  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 211  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 179  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 167  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 251  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 165  
Fragment?: true
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 110  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 167  
Fragment?: false
Publication  
First Author: Millet JK
Year: 2015
Journal: Virus Res
Title: Host cell proteases: Critical determinants of coronavirus tropism and pathogenesis.
Volume: 202
Pages: 120-34
Publication  
First Author: Coutard B
Year: 2020
Journal: Antiviral Res
Title: The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade.
Volume: 176
Pages: 104742
Publication
First Author: Shulla A
Year: 2009
Journal: J Biol Chem
Title: Role of spike protein endodomains in regulating coronavirus entry.
Volume: 284
Issue: 47
Pages: 32725-34
Protein Domain
Type: Domain
Description: The type I glycoprotein S of Coronavirus, trimers of which constitute the typical viral spikes, is assembled into virions through noncovalent interactions with the M protein. The spike glycoprotein is translated as a large polypeptide that is subsequently cleaved to S1 () and S2 []. The cleavage of S can occur at two distinct sites: S2 or S2' []. The spike is present in two very different forms: pre-fusion (the form on mature virions) and post-fusion (the form after membrane fusion has been completed). The spike is cleaved sequentially by host proteases at two sites: first at the S1/S2 boundary (i.e. S1/S2 site) and second within S2 (i.e. S2' site). After the cleavages, S1 dissociates from S2, allowing S2 to transition to the post-fusion structure []. Both chimeric S proteins appeared to cause cell fusion when expressed individually, suggesting that they were biologically fully active []. The spike is a type I membrane glycoprotein that possesses a conserved transmembrane anchor and an unusual cysteine-rich (cys) domain that bridges the putative junction of the anchor and the cytoplasmic tail [].SARS-CoV S is largely uncleaved after biosynthesis. It can be later processed by endosomal cathepsin L, trypsin, thermolysin, and elastase, which are shown to induce syncytia formation and virus entry. Other proteases that are of potential biological relevance in potentiating SARS-CoV S include TMPRSS2, TMPRSS11a, and HAT which are localized on the cell surface and are highly expressed in the human airway []. The furin-like S2' cleavage site at KR/SF with P1 and P2 basic residues and a P2' hydrophobic Phe downstream of the IFP is identical between the SARS-CoV-2 and SARS-CoV. One or more furin-like enzymes would cleave the S2' site at KR/SF [, ]. Deletion of SARS-CoV-2 furin cleavage site suggests that it may not be required for viral entry but may affect replication kinetics and altered sites have been still seen proteolytically cleaved. Several substitutions within the S2' cleavage domain of SARS-COV-2 have been reported, including P812L/S/T, S813I/G, F817L, I818S/V, but further experimental study of their consequences and the replication properties of the altered viruses are required to understand the role of furin cleavage in SARS-CoV-2 infection and virulence []. The S2 subunit normally contains multiple key components, including one or more fusion peptides (FP), a second proteolytic site (S2') and two conserved heptad repeats (HRs), driving membrane penetration and virus-cell fusion. The HRs can trimerize into a coiled-coil structure built of three HR1-HR2 helical hairpins presenting as a canonical six-helix bundle and drag the virus envelope and the host cell bilayer into close proximity, preparing for fusion to occur []. The fusion core is composed of HR1 and HR2 and at least three membranotropic regions that are denoted as the fusion peptide (FP), internal fusion peptide (IFP), and pretransmembrane domain (PTM). The HR regions are further flanked by the three membranotropic components. Both FP and IFP are located upstream of HR1, while PTM is distally downstream of HR2 and directly precedes the transmembrane domain of SARS-CoV S. All of these three components are able to partition into the phospholipid bilayer to disturb membrane integrity. []. During the pandemic, many conservative amino acid changes in FP segment of SARS-CoV-2 have been reported (i.e., L821I, L822F, K825R, V826L, T827I, L828P, A829T, D830G/A, A831V/S/T, G832C/S, F833S, I834T), although their impact is not known as the active conformation and mode of insertion of SARS-CoV-2 fusion peptide have not been experimentally characterised. Differences in HR1 sequences between SARS-CoV and SARS-CoV-2 suggest that SARS-CoV-2 HR2 makes stronger interactions with HR1. However, the substitutions observed in the solvent accessible surface of the HR1 domain (e.g., D936Y, S943P, S939F) of SARS-CoV-2 do not seem to be involved in stabilizing interactions with HR2. Substitutions in HR2 (e.g., K1073N, V1176F) or the TM or cytoplasmic tail domains have also been observed, but further experimental work is required to determine the effects of these changes [].This entry represents the cysteine rich intravirion region found at the C-terminal of coronavirus spike proteins (S) []. These cysteine residues are targets for palmitoylation, necessary for efficiently S incorporation into virions and S-mediated membrane fusions.
Protein Domain
Type: Domain
Description: The type I glycoprotein S of Coronavirus, trimers of which constitute the typical viral spikes, is assembled into virions through noncovalent interactions with the M protein. The spike glycoprotein is translated as a large polypeptide that is subsequently cleaved to S1 () and S2 []. The cleavage of S can occur at two distinct sites: S2 or S2' []. The spike is present in two very different forms: pre-fusion (the form on mature virions) and post-fusion (the form after membrane fusion has been completed). The spike is cleaved sequentially by host proteases at two sites: first at the S1/S2 boundary (i.e. S1/S2 site) and second within S2 (i.e. S2' site). After the cleavages, S1 dissociates from S2, allowing S2 to transition to the post-fusion structure []. Both chimeric S proteins appeared to cause cell fusion when expressed individually, suggesting that they were biologically fully active []. The spike is a type I membrane glycoprotein that possesses a conserved transmembrane anchor and an unusual cysteine-rich (cys) domain that bridges the putative junction of the anchor and the cytoplasmic tail [].SARS-CoV S is largely uncleaved after biosynthesis. It can be later processed by endosomal cathepsin L, trypsin, thermolysin, and elastase, which are shown to induce syncytia formation and virus entry. Other proteases that are of potential biological relevance in potentiating SARS-CoV S include TMPRSS2, TMPRSS11a, and HAT which are localized on the cell surface and are highly expressed in the human airway []. The furin-like S2' cleavage site at KR/SF with P1 and P2 basic residues and a P2' hydrophobic Phe downstream of the IFP is identical between the SARS-CoV-2 and SARS-CoV. One or more furin-like enzymes would cleave the S2' site at KR/SF [, ]. Deletion of SARS-CoV-2 furin cleavage site suggests that it may not be required for viral entry but may affect replication kinetics and altered sites have been still seen proteolytically cleaved. Several substitutions within the S2' cleavage domain of SARS-COV-2 have been reported, including P812L/S/T, S813I/G, F817L, I818S/V, but further experimental study of their consequences and the replication properties of the altered viruses are required to understand the role of furin cleavage in SARS-CoV-2 infection and virulence []. The S2 subunit normally contains multiple key components, including one or more fusion peptides (FP), a second proteolytic site (S2') and two conserved heptad repeats (HRs), driving membrane penetration and virus-cell fusion. The HRs can trimerize into a coiled-coil structure built of three HR1-HR2 helical hairpins presenting as a canonical six-helix bundle and drag the virus envelope and the host cell bilayer into close proximity, preparing for fusion to occur []. The fusion core is composed of HR1 and HR2 and at least three membranotropic regions that are denoted as the fusion peptide (FP), internal fusion peptide (IFP), and pretransmembrane domain (PTM). The HR regions are further flanked by the three membranotropic components. Both FP and IFP are located upstream of HR1, while PTM is distally downstream of HR2 and directly precedes the transmembrane domain of SARS-CoV S. All of these three components are able to partition into the phospholipid bilayer to disturb membrane integrity. []. During the pandemic, many conservative amino acid changes in FP segment of SARS-CoV-2 have been reported (i.e., L821I, L822F, K825R, V826L, T827I, L828P, A829T, D830G/A, A831V/S/T, G832C/S, F833S, I834T), although their impact is not known as the active conformation and mode of insertion of SARS-CoV-2 fusion peptide have not been experimentally characterised. Differences in HR1 sequences between SARS-CoV and SARS-CoV-2 suggest that SARS-CoV-2 HR2 makes stronger interactions with HR1. However, the substitutions observed in the solvent accessible surface of the HR1 domain (e.g., D936Y, S943P, S939F) of SARS-CoV-2 do not seem to be involved in stabilizing interactions with HR2. Substitutions in HR2 (e.g., K1073N, V1176F) or the TM or cytoplasmic tail domains have also been observed, but further experimental work is required to determine the effects of these changes [].This entry represents the heptad repeat 1 (HR1) from coronavirus Spike glycoprotein, S2 subunit. This region forms a long trimeric helical coiled-coil structure with peptides from the HR2 region packing in an oblique antiparallel manner on the grooves of the HR1 trimer in a mixed extended and helical conformation. Packing of the helical parts of HR2 on the HR1 trimer grooves and formation of a six-helical bundle plays an important role in the formation of a stable post-fusion structure. In contrast to their extended helical conformations in the post-fusion state, the HR1 motifs within S2 form several shorter helices in their pre-fusion state [, ].
Protein Domain
Type: Domain
Description: The type I glycoprotein S of Coronavirus, trimers of which constitute the typical viral spikes, is assembled into virions through noncovalent interactions with the M protein. The spike glycoprotein is translated as a large polypeptide that is subsequently cleaved to S1 () and S2 []. The cleavage of S can occur at two distinct sites: S2 or S2' []. The spike is present in two very different forms: pre-fusion (the form on mature virions) and post-fusion (the form after membrane fusion has been completed). The spike is cleaved sequentially by host proteases at two sites: first at the S1/S2 boundary (i.e. S1/S2 site) and second within S2 (i.e. S2' site). After the cleavages, S1 dissociates from S2, allowing S2 to transition to the post-fusion structure []. Both chimeric S proteins appeared to cause cell fusion when expressed individually, suggesting that they were biologically fully active []. The spike is a type I membrane glycoprotein that possesses a conserved transmembrane anchor and an unusual cysteine-rich (cys) domain that bridges the putative junction of the anchor and the cytoplasmic tail [].SARS-CoV S is largely uncleaved after biosynthesis. It can be later processed by endosomal cathepsin L, trypsin, thermolysin, and elastase, which are shown to induce syncytia formation and virus entry. Other proteases that are of potential biological relevance in potentiating SARS-CoV S include TMPRSS2, TMPRSS11a, and HAT which are localized on the cell surface and are highly expressed in the human airway []. The furin-like S2' cleavage site at KR/SF with P1 and P2 basic residues and a P2' hydrophobic Phe downstream of the IFP is identical between the SARS-CoV-2 and SARS-CoV. One or more furin-like enzymes would cleave the S2' site at KR/SF [, ]. Deletion of SARS-CoV-2 furin cleavage site suggests that it may not be required for viral entry but may affect replication kinetics and altered sites have been still seen proteolytically cleaved. Several substitutions within the S2' cleavage domain of SARS-COV-2 have been reported, including P812L/S/T, S813I/G, F817L, I818S/V, but further experimental study of their consequences and the replication properties of the altered viruses are required to understand the role of furin cleavage in SARS-CoV-2 infection and virulence []. The S2 subunit normally contains multiple key components, including one or more fusion peptides (FP), a second proteolytic site (S2') and two conserved heptad repeats (HRs), driving membrane penetration and virus-cell fusion. The HRs can trimerize into a coiled-coil structure built of three HR1-HR2 helical hairpins presenting as a canonical six-helix bundle and drag the virus envelope and the host cell bilayer into close proximity, preparing for fusion to occur []. The fusion core is composed of HR1 and HR2 and at least three membranotropic regions that are denoted as the fusion peptide (FP), internal fusion peptide (IFP), and pretransmembrane domain (PTM). The HR regions are further flanked by the three membranotropic components. Both FP and IFP are located upstream of HR1, while PTM is distally downstream of HR2 and directly precedes the transmembrane domain of SARS-CoV S. All of these three components are able to partition into the phospholipid bilayer to disturb membrane integrity. []. During the pandemic, many conservative amino acid changes in FP segment of SARS-CoV-2 have been reported (i.e., L821I, L822F, K825R, V826L, T827I, L828P, A829T, D830G/A, A831V/S/T, G832C/S, F833S, I834T), although their impact is not known as the active conformation and mode of insertion of SARS-CoV-2 fusion peptide have not been experimentally characterised. Differences in HR1 sequences between SARS-CoV and SARS-CoV-2 suggest that SARS-CoV-2 HR2 makes stronger interactions with HR1. However, the substitutions observed in the solvent accessible surface of the HR1 domain (e.g., D936Y, S943P, S939F) of SARS-CoV-2 do not seem to be involved in stabilizing interactions with HR2. Substitutions in HR2 (e.g., K1073N, V1176F) or the TM orcytoplasmic tail domains have also been observed, but further experimental work is required to determine the effects of these changes [].This entry represents the heptad repeat 2 (HR2) from coronavirus Spike glycoprotein, S2 subunit. It adopts a mixed conformation: the central part fold into a nine-turn α-helix, while the residues on either side of the helix adopt an extended conformation. Packing of the helical parts of HR2 on the HR1 trimer grooves and formation of a six-helical bundle plays an important role in the formation of a stable post-fusion structure [, ].
Publication
First Author: Sarojini S
Year: 2011
Journal: DNA Cell Biol
Title: Interferon-induced tetherin restricts vesicular stomatitis virus release in neurons.
Volume: 30
Issue: 12
Pages: 965-74
Publication
First Author: Mariathasan S
Year: 2004
Journal: Nature
Title: Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf.
Volume: 430
Issue: 6996
Pages: 213-8
Publication
First Author: Srivastava D
Year: 2012
Journal: J Mol Biol
Title: The three-dimensional structural basis of type II hyperprolinemia.
Volume: 420
Issue: 3
Pages: 176-89
Publication
First Author: Hsieh CL
Year: 2014
Journal: J Neurotrauma
Title: CCR2 deficiency impairs macrophage infiltration and improves cognitive function after traumatic brain injury.
Volume: 31
Issue: 20
Pages: 1677-88
Publication
First Author: Kasahara T
Year: 2010
Journal: Proc Natl Acad Sci U S A
Title: Genetic variation of melatonin productivity in laboratory mice under domestication.
Volume: 107
Issue: 14
Pages: 6412-7
Publication
First Author: Gosejacob D
Year: 2016
Journal: J Biol Chem
Title: Ceramide Synthase 5 Is Essential to Maintain C16:0-Ceramide Pools and Contributes to the Development of Diet-induced Obesity.
Volume: 291
Issue: 13
Pages: 6989-7003
Publication
First Author: Boerries M
Year: 2007
Journal: Mol Cell Biol
Title: Ca2+ -dependent interaction of S100A1 with F1-ATPase leads to an increased ATP content in cardiomyocytes.
Volume: 27
Issue: 12
Pages: 4365-73
Publication
First Author: Kim D
Year: 2010
Journal: J Biol Chem
Title: Enzymatic activity is required for the in vivo functions of CARM1.
Volume: 285
Issue: 2
Pages: 1147-52
Publication
First Author: Camargo SM
Year: 2009
Journal: Gastroenterology
Title: Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations.
Volume: 136
Issue: 3
Pages: 872-82
Publication
First Author: Snyder E
Year: 2020
Journal: Sci Rep
Title: ADAD1 and ADAD2, testis-specific adenosine deaminase domain-containing proteins, are required for male fertility.
Volume: 10
Issue: 1
Pages: 11536
Publication  
First Author: Baarine M
Year: 2012
Journal: Neuroscience
Title: Evidence of oxidative stress in very long chain fatty acid--treated oligodendrocytes and potentialization of ROS production using RNA interference-directed knockdown of ABCD1 and ACOX1 peroxisomal proteins.
Volume: 213
Pages: 1-18
Publication
First Author: Satoh K
Year: 2015
Journal: J Biol Chem
Title: ATP-binding cassette transporter A7 (ABCA7) loss of function alters Alzheimer amyloid processing.
Volume: 290
Issue: 40
Pages: 24152-65
Publication
First Author: Reynolds SD
Year: 2007
Journal: Am J Physiol Lung Cell Mol Physiol
Title: CCSP regulates cross talk between secretory cells and both ciliated cells and macrophages of the conducting airway.
Volume: 293
Issue: 1
Pages: L114-23
Publication
First Author: Tong F
Year: 2010
Journal: J Biol Chem
Title: Decreased expression of ARV1 results in cholesterol retention in the endoplasmic reticulum and abnormal bile acid metabolism.
Volume: 285
Issue: 44
Pages: 33632-41
Publication
First Author: Ercan-Sencicek AG
Year: 2015
Journal: Eur J Hum Genet
Title: Homozygous loss of DIAPH1 is a novel cause of microcephaly in humans.
Volume: 23
Issue: 2
Pages: 165-72
Publication
First Author: Zhu H
Year: 2007
Journal: Birth Defects Res A Clin Mol Teratol
Title: Cardiovascular abnormalities in Folr1 knockout mice and folate rescue.
Volume: 79
Issue: 4
Pages: 257-68
Publication
First Author: Latour S
Year: 1996
Journal: J Biol Chem
Title: Differential intrinsic enzymatic activity of Syk and Zap-70 protein-tyrosine kinases.
Volume: 271
Issue: 37
Pages: 22782-90
Publication
First Author: Cortez VS
Year: 2014
Journal: J Exp Med
Title: CRTAM controls residency of gut CD4+CD8+ T cells in the steady state and maintenance of gut CD4+ Th17 during parasitic infection.
Volume: 211
Issue: 4
Pages: 623-33
Publication
First Author: Praslickova D
Year: 2012
Journal: PLoS One
Title: The ileal lipid binding protein is required for efficient absorption and transport of bile acids in the distal portion of the murine small intestine.
Volume: 7
Issue: 12
Pages: e50810
Publication
First Author: Sepúlveda MR
Year: 2009
Journal: J Neurosci
Title: Silencing the SPCA1 (secretory pathway Ca2+-ATPase isoform 1) impairs Ca2+ homeostasis in the Golgi and disturbs neural polarity.
Volume: 29
Issue: 39
Pages: 12174-82
Publication
First Author: Zuo Y
Year: 2008
Journal: J Biol Chem
Title: ABCA12 maintains the epidermal lipid permeability barrier by facilitating formation of ceramide linoleic esters.
Volume: 283
Issue: 52
Pages: 36624-35
Publication
First Author: Abu-Elheiga L
Year: 2003
Journal: Proc Natl Acad Sci U S A
Title: Acetyl-CoA carboxylase 2 mutant mice are protected against obesity and diabetes induced by high-fat/high-carbohydrate diets.
Volume: 100
Issue: 18
Pages: 10207-12
Publication
First Author: Yoshikawa F
Year: 2016
Journal: PLoS One
Title: Mammalian-Specific Central Myelin Protein Opalin Is Redundant for Normal Myelination: Structural and Behavioral Assessments.
Volume: 11
Issue: 11
Pages: e0166732
Publication
First Author: Allen NP
Year: 2007
Journal: Oncogene
Title: RASSF6 is a novel member of the RASSF family of tumor suppressors.
Volume: 26
Issue: 42
Pages: 6203-11
Publication
First Author: Nola S
Year: 2008
Journal: Hum Mol Genet
Title: Scrib regulates PAK activity during the cell migration process.
Volume: 17
Issue: 22
Pages: 3552-65
Publication
First Author: Harris TP
Year: 2014
Journal: G3 (Bethesda)
Title: IQ motif-containing G (Iqcg) is required for mouse spermiogenesis.
Volume: 4
Issue: 2
Pages: 367-72
Publication
First Author: Parra JL
Year: 2005
Journal: J Biol Chem
Title: Features of the catalytic domains and C termini of the MAPK signal-integrating kinases Mnk1 and Mnk2 determine their differing activities and regulatory properties.
Volume: 280
Issue: 45
Pages: 37623-33
Publication
First Author: Durlinger AL
Year: 2001
Journal: Endocrinology
Title: Anti-Müllerian hormone attenuates the effects of FSH on follicle development in the mouse ovary.
Volume: 142
Issue: 11
Pages: 4891-9
Publication
First Author: Xie J
Year: 2004
Journal: Proc Natl Acad Sci U S A
Title: Absence of a reductase, NCB5OR, causes insulin-deficient diabetes.
Volume: 101
Issue: 29
Pages: 10750-5
Publication
First Author: Pan H
Year: 2015
Journal: PLoS One
Title: Translational Initiation at a Non-AUG Start Codon for Human and Mouse Negative Elongation Factor-B.
Volume: 10
Issue: 5
Pages: e0127422
Publication
First Author: Scott F
Year: 2017
Journal: Drug Metab Dispos
Title: Identification of Flavin-Containing Monooxygenase 5 (FMO5) as a Regulator of Glucose Homeostasis and a Potential Sensor of Gut Bacteria.
Volume: 45
Issue: 9
Pages: 982-989
Publication  
First Author: Varshavi D
Year: 2018
Journal: Front Mol Biosci
Title: Metabolic Biomarkers of Ageing in C57BL/6J Wild-Type and Flavin-Containing Monooxygenase 5 (FMO5)-Knockout Mice.
Volume: 5
Pages: 28
Publication
First Author: Meguenani M
Year: 2015
Journal: FASEB J
Title: Junctional adhesion molecule B interferes with angiogenic VEGF/VEGFR2 signaling.
Volume: 29
Issue: 8
Pages: 3411-25
Publication
First Author: Day CL
Year: 2005
Journal: J Biol Chem
Title: Solution structure of prosurvival Mcl-1 and characterization of its binding by proapoptotic BH3-only ligands.
Volume: 280
Issue: 6
Pages: 4738-44
Publication
First Author: Gronert K
Year: 2005
Journal: J Biol Chem
Title: A role for the mouse 12/15-lipoxygenase pathway in promoting epithelial wound healing and host defense.
Volume: 280
Issue: 15
Pages: 15267-78
Publication
First Author: Deng L
Year: 2008
Journal: Mol Genet Metab
Title: Methionine synthase reductase deficiency results in adverse reproductive outcomes and congenital heart defects in mice.
Volume: 94
Issue: 3
Pages: 336-42
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First Author: Mistrík P
Year: 2005
Journal: J Biol Chem
Title: The murine HCN3 gene encodes a hyperpolarization-activated cation channel with slow kinetics and unique response to cyclic nucleotides.
Volume: 280
Issue: 29
Pages: 27056-61
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First Author: Chong YC
Year: 2015
Journal: Genes Dev
Title: Bifurcating action of Smoothened in Hedgehog signaling is mediated by Dlg5.
Volume: 29
Issue: 3
Pages: 262-76
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First Author: Chan KM
Year: 2012
Journal: J Biol Chem
Title: Leucine-rich repeat and WD repeat-containing protein 1 is recruited to pericentric heterochromatin by trimethylated lysine 9 of histone H3 and maintains heterochromatin silencing.
Volume: 287
Issue: 18
Pages: 15024-33
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First Author: Hodgkinson VL
Year: 2015
Journal: J Pathol
Title: X-linked spinal muscular atrophy in mice caused by autonomous loss of ATP7A in the motor neuron.
Volume: 236
Issue: 2
Pages: 241-50
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First Author: Haffner-Luntzer M
Year: 2014
Journal: PLoS One
Title: Midkine-deficiency delays chondrogenesis during the early phase of fracture healing in mice.
Volume: 9
Issue: 12
Pages: e116282
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First Author: Ohmae S
Year: 2006
Journal: J Biol Chem
Title: Molecular identification and characterization of a family of kinases with homology to Ca2+/calmodulin-dependent protein kinases I/IV.
Volume: 281
Issue: 29
Pages: 20427-39
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First Author: Loo YM
Year: 2008
Journal: J Virol
Title: Distinct RIG-I and MDA5 signaling by RNA viruses in innate immunity.
Volume: 82
Issue: 1
Pages: 335-45
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First Author: Miller KA
Year: 2013
Journal: PLoS Genet
Title: Cauli: a mouse strain with an Ift140 mutation that results in a skeletal ciliopathy modelling Jeune syndrome.
Volume: 9
Issue: 8
Pages: e1003746
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First Author: Ingram JL
Year: 2006
Journal: J Immunol
Title: Opposing actions of Stat1 and Stat6 on IL-13-induced up-regulation of early growth response-1 and platelet-derived growth factor ligands in pulmonary fibroblasts.
Volume: 177
Issue: 6
Pages: 4141-8
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First Author: Sun H
Year: 2012
Journal: Arterioscler Thromb Vasc Biol
Title: Proprotein convertase subtilisin/kexin type 9 interacts with apolipoprotein B and prevents its intracellular degradation, irrespective of the low-density lipoprotein receptor.
Volume: 32
Issue: 7
Pages: 1585-95
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First Author: Tanner JJ
Year: 2016
Journal: Biochemistry
Title: EF5 Is the High-Affinity Mg(2+) Site in ALG-2.
Volume: 55
Issue: 36
Pages: 5128-41
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First Author: Morais VA
Year: 2009
Journal: EMBO Mol Med
Title: Parkinson's disease mutations in PINK1 result in decreased Complex I activity and deficient synaptic function.
Volume: 1
Issue: 2
Pages: 99-111
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First Author: Zou W
Year: 2007
Journal: J Cell Biol
Title: Syk, c-Src, the alphavbeta3 integrin, and ITAM immunoreceptors, in concert, regulate osteoclastic bone resorption.
Volume: 176
Issue: 6
Pages: 877-88
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First Author: Dirkx R
Year: 2005
Journal: Hepatology
Title: Absence of peroxisomes in mouse hepatocytes causes mitochondrial and ER abnormalities.
Volume: 41
Issue: 4
Pages: 868-78
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First Author: Lerch-Gaggl AF
Year: 2007
Journal: J Biol Chem
Title: Light chain 1 of microtubule-associated protein 1B can negatively regulate the action of Pes1.
Volume: 282
Issue: 15
Pages: 11308-16
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First Author: Tanaka KI
Year: 2018
Journal: Proc Natl Acad Sci U S A
Title: FAM210A is a novel determinant of bone and muscle structure and strength.
Volume: 115
Issue: 16
Pages: E3759-E3768