MouseMine: Keyword Search

Publication

First Author:	Cumberbatch M
Year:	1996
Journal:	Immunology
Title:	Constitutive and inducible expression of interleukin-6 by Langerhans cells and lymph node dendritic cells.
Volume:	87
Issue:	4
Pages:	513-8

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Publication

8792611 | J:36130

First Author:	Wood HB
Year:	1996
Journal:	Dev Genet
Title:	Effects of all-trans-retinoic acid on skeletal pattern, 5'HoxD gene expression, and RAR beta 2/beta 4 promoter activity in embryonic mouse limbs.
Volume:	19
Issue:	1
Pages:	74-84

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Publication

8937451 | J:36221

First Author:	Constantin D
Year:	1996
Journal:	Biochem Pharmacol
Title:	Uroporphyria induced by 5-aminolaevulinic acid alone in Ahrd SWR mice.
Volume:	52
Issue:	9
Pages:	1407-13

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Publication

8943044 | J:37051

First Author:	Hancock WW
Year:	1996
Journal:	Proc Natl Acad Sci U S A
Title:	Costimulatory function and expression of CD40 ligand, CD80, and CD86 in vascularized murine cardiac allograft rejection.
Volume:	93
Issue:	24
Pages:	13967-72

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Publication

9015189 | J:37639

First Author:	Li XC
Year:	1997
Journal:	Cell Immunol
Title:	Expression of functional ICAM-1 and VCAM-1 adhesion molecules by an immortalized epithelial cell clone derived from the small intestine.
Volume:	175
Issue:	1
Pages:	58-66

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Publication

9094091 | J:39388

First Author:	Geum D
Year:	1997
Journal:	Mol Reprod Dev
Title:	Estrogen-induced cyclin D1 and D3 gene expressions during mouse uterine cell proliferation in vivo: differential induction mechanism of cyclin D1 and D3.
Volume:	46
Issue:	4
Pages:	450-8

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Publication

9186055 | J:40797

First Author:	Webb SE
Year:	1997
Journal:	Dev Dyn
Title:	Fibroblast growth factors 2 and 4 stimulate migration of mouse embryonic limb myogenic cells.
Volume:	209
Issue:	2
Pages:	206-16

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Publication

9219835 | J:41393

First Author:	Allémann E
Year:	1997
Journal:	Int J Cancer
Title:	Photodynamic activities and biodistribution of fluorinated zinc phthalocyanine derivatives in the murine EMT-6 tumour model.
Volume:	72
Issue:	2
Pages:	289-94

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Publication

9260924 | J:42084

First Author:	Mallick S
Year:	1997
Journal:	DNA Cell Biol
Title:	Transcriptional regulation of the murine multidrug resistance gene mdr1b by progesterone occurs via an indirect mechanism.
Volume:	16
Issue:	7
Pages:	807-18

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Publication

9356174 | J:44228

First Author:	Tenbroek EM
Year:	1997
Journal:	Dev Biol
Title:	The differential effects of 12-O-tetradecanoylphorbol-13-acetate on the gap junctions and connexins of the developing mammalian lens.
Volume:	191
Issue:	1
Pages:	88-102

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Publication

9389458 | J:44062

First Author:	Arai A
Year:	1997
Journal:	Dev Dyn
Title:	Murine cardiac progenitor cells require visceral embryonic endoderm and primitive streak for terminal differentiation.
Volume:	210
Issue:	3
Pages:	344-53

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Publication

9433804 | J:45161

First Author:	Songsasen N
Year:	1998
Journal:	J Exp Zool
Title:	Birth of live mice derived by in vitro fertilization with spermatozoa retrieved up to twenty-four hours after death.
Volume:	280
Issue:	2
Pages:	189-96

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Publication

9671750 | J:49342

First Author:	Varin-Blank N
Year:	1998
Journal:	Proc Natl Acad Sci U S A
Title:	Male-specific transcription initiation of the C4-Slp gene in mouse liver follows activation of STAT5.
Volume:	95
Issue:	15
Pages:	8750-5

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Publication

9731754 | J:52670

First Author:	Burd R
Year:	1998
Journal:	J Cell Physiol
Title:	Tumor cell apoptosis, lymphocyte recruitment and tumor vascular changes are induced by low temperature, long duration (fever-like) whole body hyperthermia.
Volume:	177
Issue:	1
Pages:	137-47

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Publication

9835280 | J:51456

First Author:	Radcliffe RA
Year:	1998
Journal:	Alcohol Clin Exp Res
Title:	Acute functional tolerance to ethanol and fear conditioning are genetically correlated in mice.
Volume:	22
Issue:	8
Pages:	1673-9

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Publication

9839358 | J:51265

First Author:	Degitz SJ
Year:	1998
Journal:	Teratology
Title:	Role of TGF-beta in RA-induced cleft palate in CD-1 mice.
Volume:	58
Issue:	5
Pages:	197-204

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Publication

9894676 | J:52258

First Author:	Mulder GB
Year:	1998
Journal:	Teratology
Title:	Retinoic acid-induced thymic abnormalities in the mouse are associated with altered pharyngeal morphology, thymocyte maturation defects, and altered expression of Hoxa3 and Pax1.
Volume:	58
Issue:	6
Pages:	263-75

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Publication

10397285 | J:56175

First Author:	Grahame NJ
Year:	1999
Journal:	Alcohol Clin Exp Res
Title:	Limited access alcohol drinking in high- and low-alcohol preferring selected lines of mice.
Volume:	23
Issue:	6
Pages:	1015-22

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Publication

10443996 | J:56968

First Author:	Ryabinin AE
Year:	1999
Journal:	Alcohol Clin Exp Res
Title:	Selective effects of alcohol drinking on restraint-induced expression of immediate early genes in mouse brain.
Volume:	23
Issue:	7
Pages:	1272-80

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Publication

10457215 | J:56703

First Author:	Cao X
Year:	1999
Journal:	Immunology
Title:	Therapy of established tumour with a hybrid cellular vaccine generated by using granulocyte-macrophage colony-stimulating factor genetically modified dendritic cells.
Volume:	97
Issue:	4
Pages:	616-25

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Publication

11796704 | J:75188

First Author:	Tankersley CG
Year:	2002
Journal:	J Appl Physiol (1985)
Title:	Circadian rhythm variation in activity, body temperature, and heart rate between C3H/HeJ and C57BL/6J inbred strains.
Volume:	92
Issue:	2
Pages:	870-7

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Publication

11835573 | J:79413

First Author:	Williams JW
Year:	2002
Journal:	Mol Reprod Dev
Title:	Trophectoderm-specific expression of the X-linked Bex1/Rex3 gene in preimplantation stage mouse embryos.
Volume:	61
Issue:	3
Pages:	281-7

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Publication

12388436 | J:82498

First Author:	Tankersley CG
Year:	2003
Journal:	Am J Physiol Regul Integr Comp Physiol
Title:	Unstable heart rate and temperature regulation predict mortality in AKR/J mice.
Volume:	284
Issue:	3
Pages:	R742-50

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Publication

16020276 | J:101095

First Author:	Kase S
Year:	2005
Journal:	Curr Eye Res
Title:	Disappearance of p27(KIP1) and increase in proliferation of the lens cells after extraction of most of the fiber cells of the lens.
Volume:	30
Issue:	6
Pages:	437-42

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Publication

16683987 | J:108191

First Author:	Jochheim-Richter A
Year:	2006
Journal:	Differentiation
Title:	Gene expression analysis identifies novel genes participating in early murine liver development and adult liver regeneration.
Volume:	74
Issue:	4
Pages:	167-73

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Publication

1160223 | J:109966

First Author:	Stein JH
Year:	1975
Journal:	Kidney Int
Title:	Pathophysiology of a nephrotoxic model of acute renal failure.
Volume:	8
Issue:	1
Pages:	27-41

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Publication

16878317 | J:116005

First Author:	Bidinotto LT
Year:	2006
Journal:	Environ Mol Mutagen
Title:	Effects of ginger (Zingiber officinale Roscoe) on DNA damage and development of urothelial tumors in a mouse bladder carcinogenesis model.
Volume:	47
Issue:	8
Pages:	624-30

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Publication

12637351 | J:133056

First Author:	Kirchhof P
Year:	2003
Journal:	Am J Physiol Heart Circ Physiol
Title:	Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A1 adenosine receptor.
Volume:	285
Issue:	1
Pages:	H145-53

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Publication

15467015 | J:133744

First Author:	Sakai K
Year:	2004
Journal:	Physiol Genomics
Title:	Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II.
Volume:	20
Issue:	1
Pages:	66-72

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Publication

19177162 | J:144821

First Author:	Touma C
Year:	2009
Journal:	PLoS One
Title:	Rhythmicity in mice selected for extremes in stress reactivity: behavioural, endocrine and sleep changes resembling endophenotypes of major depression.
Volume:	4
Issue:	1
Pages:	e4325

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Publication

20704734 | J:163833

First Author:	Tsai TC
Year:	2010
Journal:	BMC Dev Biol
Title:	Granzyme G is expressed in the two-cell stage mouse embryo and is required for the maternal-zygotic transition.
Volume:	10

Pages:	88

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Publication

22960454 | J:189239

First Author:	Azer J
Year:	2012
Journal:	J Mol Cell Cardiol
Title:	Natriuretic peptides regulate heart rate and sinoatrial node function by activating multiple natriuretic peptide receptors.
Volume:	53
Issue:	5
Pages:	715-24

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Publication

22916088 | J:190056

First Author:	Xu Y
Year:	2012
Journal:	PLoS One
Title:	Transcriptional programs controlling perinatal lung maturation.
Volume:	7
Issue:	8
Pages:	e37046

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Publication

23505536 | J:199924

First Author:	Sproull M
Year:	2013
Journal:	PLoS One
Title:	Correlation of plasma FL expression with bone marrow irradiation dose.
Volume:	8
Issue:	3
Pages:	e58558

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Publication

23560112 | J:200152

First Author:	Tuominen I
Year:	2013
Journal:	PLoS One
Title:	Diet-induced obesity promotes colon tumor development in azoxymethane-treated mice.
Volume:	8
Issue:	4
Pages:	e60939

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Publication

25428949 | J:228849

First Author:	Tank J
Year:	2014
Journal:	Physiol Rep
Title:	Preserved functional autonomic phenotype in adult mice overexpressing moderate levels of human alpha-synuclein in oligodendrocytes.
Volume:	2
Issue:	11

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Publication

26020792 | J:237734

First Author:	Gaskill BN
Year:	2015
Journal:	PLoS One
Title:	The Effect of Cage Space on Behavior and Reproduction in Crl:CD1(Icr) and C57BL/6NCrl Laboratory Mice.
Volume:	10
Issue:	5
Pages:	e0127875

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Publication

28207794 | J:248510

First Author:	Castillo GM
Year:	2017
Journal:	PLoS One
Title:	Protected graft copolymer-formulated fibroblast growth factors mitigate the lethality of partial body irradiation injury.
Volume:	12
Issue:	2
Pages:	e0171703

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Publication

28464043 | J:247987

First Author:	d'Anglemont de Tassigny X
Year:	2017
Journal:	PLoS One
Title:	Mechanistic insights into the more potent effect of KP-54 compared to KP-10 in vivo.
Volume:	12
Issue:	5
Pages:	e0176821

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Publication

26925974 | J:259814

First Author:	Schéle E
Year:	2016
Journal:	PLoS One
Title:	Centrally Administered Ghrelin Acutely Influences Food Choice in Rodents.
Volume:	11
Issue:	2
Pages:	e0149456

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Publication

18465999 | J:49705

First Author:	Roudebush WE
Year:	1998
Journal:	Zoolog Sci
Title:	Influence of the preimplantation-embryo-development (ped) gene on mouse blastocyst differentiation.
Volume:	15
Issue:	3
Pages:	359-62

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Publication

6839348 | J:280983

First Author:	Molls M
Year:	1983
Journal:	Cell Tissue Kinet
Title:	A comparison of the cell kinetics of pre-implantation mouse embryos from two different mouse strains.
Volume:	16
Issue:	3
Pages:	277-83

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Publication

4553851 | J:292880

First Author:	Biozzi G
Year:	1972
Journal:	J Exp Med
Title:	Cytodynamics of the immune response in two lines of mice genetically selected for "high" and "low" antibody synthesis.
Volume:	135
Issue:	5
Pages:	1071-94

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Publication

33206637 | J:298618

First Author:	Martínez-Marchal A
Year:	2020
Journal:	PLoS Genet
Title:	The DNA damage response is required for oocyte cyst breakdown and follicle formation in mice.
Volume:	16
Issue:	11
Pages:	e1009067

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Publication

33244052 | J:299706

First Author:	Aleksenko L
Year:	2020
Journal:	Sci Rep
Title:	Pregnant alpha-1-microglobulin (A1M) knockout mice exhibit features of kidney and placental damage, hemodynamic changes and intrauterine growth restriction.
Volume:	10
Issue:	1
Pages:	20625

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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

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First Author:	Hauck SJ
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First Author:	Shearn CT
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