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Search results 4001 to 4066 out of 4066 for Hr

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Type Details Score
Publication
- | J:13781
 
First Author: Cumming RB
Year: 1978
Journal: Mouse News Lett
Title: Multiple forms of formamidase in the mouse
Volume: 59
Pages: 47
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Publication
11689437 | -
First Author: Suzuki K
Year: 2001
Journal: EMBO J
Title: The pre-autophagosomal structure organized by concerted functions of APG genes is essential for autophagosome formation.
Volume: 20
Issue: 21
Pages: 5971-81
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Publication
29458023 | -
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
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Publication
30198895 | -
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
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Publication
17151600 | J:161766
First Author: Lein ES
Year: 2007
Journal: Nature
Title: Genome-wide atlas of gene expression in the adult mouse brain.
Volume: 445
Issue: 7124
Pages: 168-76
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Publication
25445340 | -
 
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
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Publication
32057769 | -
 
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
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Publication
19801669 | -
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
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Protein Domain
IPR043614 | Spike_S2_CoV_C
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.
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Protein Domain
IPR044873 | Spike_S2_CoV_HR1
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 [, ].
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Protein Domain
IPR044874 | Spike_S2_CoV_HR2
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 [, ].
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Publication
22253858 | J:184312
First Author: Tchorz JS
Year: 2012
Journal: PLoS One
Title: A modified RMCE-compatible Rosa26 locus for the expression of transgenes from exogenous promoters.
Volume: 7
Issue: 1
Pages: e30011
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Publication
1513324 | J:2803
First Author: Martell KJ
Year: 1992
Journal: Mol Pharmacol
Title: Cloned mouse N-acetyltransferases: enzymatic properties of expressed Nat-1 and Nat-2 gene products.
Volume: 42
Issue: 2
Pages: 265-72
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Publication
12619135 | J:82210
First Author: Ozbun LL
Year: 2003
Journal: Dev Dyn
Title: Differentially expressed nucleolar TGF-beta1 target (DENTT) in mouse development.
Volume: 226
Issue: 3
Pages: 491-511
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Publication
12963798 | J:105387
First Author: Masuki S
Year: 2003
Journal: J Physiol
Title: Impaired arterial pressure regulation during exercise due to enhanced muscular vasodilatation in calponin knockout mice.
Volume: 553
Issue: Pt 1
Pages: 203-12
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Publication
11395925 | J:103286
First Author: Hauck SJ
Year: 2001
Journal: Exp Biol Med (Maywood)
Title: Reduced levels of thyroid hormones, insulin, and glucose, and lower body core temperature in the growth hormone receptor/binding protein knockout mouse.
Volume: 226
Issue: 6
Pages: 552-8
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Publication
20634895 | J:163114
First Author: Zhang X
Year: 2010
Journal: PLoS One
Title: Altered neurocircuitry in the dopamine transporter knockout mouse brain.
Volume: 5
Issue: 7
Pages: e11506
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Publication
31275103 | J:311162
 
First Author: Moen JM
Year: 2019
Journal: Front Neurosci
Title: Overexpression of a Neuronal Type Adenylyl Cyclase (Type 8) in Sinoatrial Node Markedly Impacts Heart Rate and Rhythm.
Volume: 13
Pages: 615
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Publication
7994754 | J:21893
First Author: Pope BL
Year: 1994
Journal: Cell Immunol
Title: Murine strain variation in the natural killer cell and proliferative responses to the immunostimulatory compound 7-allyl-8-oxoguanosine: role of cytokines.
Volume: 159
Issue: 2
Pages: 194-210
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Publication
10536674 | J:59693
First Author: Melo LG
Year: 1999
Journal: Cardiovasc Res
Title: Chronic regulation of arterial blood pressure in ANP transgenic and knockout mice: role of cardiovascular sympathetic tone.
Volume: 43
Issue: 2
Pages: 437-44
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Publication
37942483 | J:342421
 
First Author: Zheng S
Year: 2023
Journal: Front Pharmacol
Title: Apelin receptor inhibition in ischemia-reperfused mouse hearts protected by endogenous n-3 polyunsaturated fatty acids.
Volume: 14
Pages: 1145413
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Publication
29107282 | J:262277
First Author: Baggio LL
Year: 2017
Journal: Mol Metab
Title: The autonomic nervous system and cardiac GLP-1 receptors control heart rate in mice.
Volume: 6
Issue: 11
Pages: 1339-1349
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Publication
33551824 | J:302836
 
First Author: Bidaud I
Year: 2020
Journal: Front Physiol
Title: Genetic Ablation of G Protein-Gated Inwardly Rectifying K+ Channels Prevents Training-Induced Sinus Bradycardia.
Volume: 11
Pages: 519382
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Publication
21486799 | J:185248
First Author: Cummings KJ
Year: 2011
Journal: J Physiol
Title: Brainstem serotonin deficiency in the neonatal period: autonomic dysregulation during mild cold stress.
Volume: 589
Issue: Pt 8
Pages: 2055-64
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Publication
8026630 | J:19197
First Author: Scott WJ
Year: 1994
Journal: Dev Biol
Title: Enhanced expression of limb malformations and axial skeleton alterations in legless mutants by transplacental exposure to retinoic acid.
Volume: 164
Issue: 1
Pages: 277-89
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Publication
7883868 | J:22585
First Author: Jaskoll T
Year: 1994
Journal: J Craniofac Genet Dev Biol
Title: Glucocorticoids, TGF-beta, and embryonic mouse salivary gland morphogenesis.
Volume: 14
Issue: 4
Pages: 217-30
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Publication
8106564 | J:16650
First Author: Pendergrass WR
Year: 1994
Journal: J Cell Physiol
Title: Murine temperature-sensitive DNA polymerase alpha mutant displays a diminished capacity to stimulate DNA synthesis in senescent human fibroblast nuclei in heterokaryons at the nonpermissive condition.
Volume: 158
Issue: 2
Pages: 270-6
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Publication
9832432 | J:51466
First Author: Weiss RE
Year: 1998
Journal: Endocrinology
Title: Thyroid hormone action on liver, heart, and energy expenditure in thyroid hormone receptor beta-deficient mice.
Volume: 139
Issue: 12
Pages: 4945-52
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Publication
11242593 | J:70050
First Author: Butz GM
Year: 2001
Journal: Physiol Genomics
Title: Long-term telemetric measurement of cardiovascular parameters in awake mice: a physiological genomics tool.
Volume: 5
Issue: 2
Pages: 89-97
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Publication
11283970 | J:68627
First Author: Mirkes PE
Year: 2001
Journal: Teratology
Title: Co-localization of active caspase-3 and DNA fragmentation (TUNEL) in normal and hyperthermia-induced abnormal mouse development.
Volume: 63
Issue: 3
Pages: 134-43
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Publication
11122450 | J:66449
First Author: Walsh WE Jr
Year: 2000
Journal: Immunology
Title: Distribution of, and immune response to, chicken anti-alpha Gal immunoglobulin Y antibodies in wild-type and alpha Gal knockout mice.
Volume: 101
Issue: 4
Pages: 467-73
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Publication
7357602 | J:6270
First Author: Suzuki S
Year: 1980
Journal: Cell
Title: Fv-2 locus controls the proportion of erythropoietic progenitor cells (BFU-E) synthesizing DNA in normal mice.
Volume: 19
Issue: 1
Pages: 225-36
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Publication
3400097 | J:27960
First Author: Lubek BM
Year: 1988
Journal: Toxicol Appl Pharmacol
Title: Metabolic evidence for the involvement of enzymatic bioactivation in the cataractogenicity of acetaminophen in genetically susceptible (C57BL/6) and resistant (DBA/2) murine strains.
Volume: 94
Issue: 3
Pages: 487-95
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Publication
1585362 | J:1354
First Author: Kanekal S
Year: 1992
Journal: Toxicol Appl Pharmacol
Title: Pharmacokinetics, metabolic activation, and lung toxicity of cyclophosphamide in C57/B16 and ICR mice.
Volume: 114
Issue: 1
Pages: 1-8
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Publication
8470112 | J:4995
First Author: Choudhuri S
Year: 1993
Journal: Toxicol Appl Pharmacol
Title: Differential expression of the metallothionein gene in liver and brain of mice and rats.
Volume: 119
Issue: 1
Pages: 1-10
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Publication
8016743 | J:17139
First Author: Abbott BD
Year: 1994
Journal: Teratology
Title: Effects of methanol on embryonic mouse palate in serum-free organ culture.
Volume: 49
Issue: 2
Pages: 122-34
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Publication
7530664 | J:20593
First Author: Sparrow JR
Year: 1994
Journal: Exp Eye Res
Title: Cytokine regulation of nitric oxide synthase in mouse retinal pigment epithelial cells in culture.
Volume: 59
Issue: 2
Pages: 129-39
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Publication
7743553 | J:25293
First Author: Rosati E
Year: 1995
Journal: Cell Immunol
Title: Cytokine response to inactivated Candida albicans in mice.
Volume: 162
Issue: 2
Pages: 256-64
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Publication
8613787 | J:30450
First Author: Ross ME
Year: 1996
Journal: J Neurosci
Title: MN20, a D2 cyclin, is transiently expressed in selected neural populations during embryogenesis.
Volume: 16
Issue: 1
Pages: 210-9
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Publication
8619889 | J:31480
First Author: Enan E
Year: 1996
Journal: Biochem Pharmacol
Title: Deltamethrin-induced thymus atrophy in male Balb/c mice.
Volume: 51
Issue: 4
Pages: 447-54
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Publication
8675612 | J:31916
First Author: Miyake T
Year: 1996
Journal: J Craniofac Genet Dev Biol
Title: Detailed staging of inbred C57BL/6 mice between Theiler's [1972] stages 18 and 21 (11-13 days of gestation) based on craniofacial development.
Volume: 16
Issue: 1
Pages: 1-31
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Publication
8985939 | J:39688
First Author: Hober D
Year: 1996
Journal: Microbiol Immunol
Title: Coxsackievirus B3-induced chronic myocarditis in mouse: use of whole blood culture to study the activation of TNF alpha-producing cells.
Volume: 40
Issue: 11
Pages: 837-45
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Publication
9268592 | J:44772
First Author: Cao W
Year: 1997
Journal: Exp Eye Res
Title: Mechanical injury increases bFGF and CNTF mRNA expression in the mouse retina.
Volume: 65
Issue: 2
Pages: 241-8
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Publication
9344887 | J:44562
First Author: McKenna IM
Year: 1997
Journal: Toxicol Appl Pharmacol
Title: Comparison of inflammatory lung responses in Wistar rats and C57 and DBA mice following acute exposure to cadmium oxide fumes.
Volume: 146
Issue: 2
Pages: 196-206
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Publication
9380021 | J:43953
First Author: Sinal CJ
Year: 1997
Journal: Mol Pharmacol
Title: Aryl hydrocarbon receptor-dependent induction of cyp1a1 by bilirubin in mouse hepatoma hepa 1c1c7 cells.
Volume: 52
Issue: 4
Pages: 590-9
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Publication
12003817 | J:77570
First Author: Zuurbier CJ
Year: 2002
Journal: Am J Physiol Heart Circ Physiol
Title: Hemodynamics of anesthetized ventilated mouse models: aspects of anesthetics, fluid support, and strain.
Volume: 282
Issue: 6
Pages: H2099-105
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Publication
12486767 | J:80911
First Author: Mao GE
Year: 2002
Journal: Teratology
Title: Quantification and localization of expression of the retinoic acid receptor-beta and -gamma mRNA isoforms during neurulation in mouse embryos with or without spina bifida.
Volume: 66
Issue: 6
Pages: 331-43
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Publication
28358847 | J:245917
First Author: Feng YL
Year: 2017
Journal: PLoS One
Title: Alpha-1-antitrypsin suppresses oxidative stress in preeclampsia by inhibiting the p38MAPK signaling pathway: An in vivo and in vitro study.
Volume: 12
Issue: 3
Pages: e0173711
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Publication
30729109 | J:284345
 
First Author: Jara ZP
Year: 2018
Journal: Front Med (Lausanne)
Title: Tonin Overexpression in Mice Diminishes Sympathetic Autonomic Modulation and Alters Angiotensin Type 1 Receptor Response.
Volume: 5
Pages: 365
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Publication
31077320 | J:283270
First Author: Gallardo M
Year: 2020
Journal: J Natl Cancer Inst
Title: Uncovering the Role of RNA-Binding Protein hnRNP K in B-Cell Lymphomas.
Volume: 112
Issue: 1
Pages: 95-106
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Publication
17036336 | J:294520
First Author: Bittel DC
Year: 2007
Journal: Am J Med Genet A
Title: Whole genome microarray analysis of gene expression in an imprinting center deletion mouse model of Prader-Willi syndrome.
Volume: 143A
Issue: 5
Pages: 422-9
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Publication
16205358 | J:338713
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