A1, A2, A3, A4, A5, A6, A7, A8, B1, B2, B3, B4
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA749649 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15368405_1.fastq.gz | Fastqsanger.gz | |||
| SRR15368405_2.fastq.gz | Fastqsanger.gz | |||
| SRR15368406_1.fastq.gz | Fastqsanger.gz | |||
| SRR15368406_2.fastq.gz | Fastqsanger.gz | |||
| SRR15368407_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Initiation of mineralisation during endochondral ossification is a multistep process and was assumed to correlate with specific interactions of annexins and collagens. Annexins A5 and A6 are postulated to represent the essential annexins promoting cartilage mineralisation. However, skeletal development appears to be normal in annexin A5 or A6 deficient mice. The highly conserved structures of annexins led to the assumption that annexins A5 and A6 may fulfill redundant functions. We now generated mice deficient for both proteins, annexins A5 and A6. Mice were viable, fertile and showed no obvious abnormalities. Assessment of skeletal elements using histological, ultrastructural and peripheral quantitative computed tomography methods revealed that mineralisation and development of the skeleton was not significantly affected in mutant mice. In respect of the lack of an obvious phenotype we now applied microarray analysis to the growth plate to define changes in the transcriptome of juvenile murine growth plates from mutant mice. Global gene expression analysis revealed subtle phenotypes at the transcriptome level of genes involved in cell growth and intermediate metabolism in mutant mice. These data demonstrate that both annexins are dispensable for proper cartilage mineralisation but may affect cell proliferation processes at the transcriptomic level.
2009-02-17 | E-MEXP-1718 | biostudies-arrayexpress
Project description:MAPK cascade in solution (no scaffold)
Description
This model describes a basic 3-
stage Mitogen Activated Protein Kinase (MAPK)
cascade in solution. This cascade is typically expressed as RAF=
=>MEK==>MAPK (alternative forms are K3==>K2==>
K1 and KKK==>KK==>K)
. The input signal is RAFK (RAF Kinase)
and the output signal is MAPKpp (
doubly phosphorylated form of MAPK)
. RAFK phosphorylates RAF once to RAFp. RAFp,
the phosphorylated form of RAF induces two phoshporylations of MEK,
to MEKp and MEKpp. MEKpp,
the doubly phosphorylated form of MEK,
induces two phosphorylations of MAPK to MAPKp and MAPKpp.
Rate constant
Reaction
a10 = 5.
MAPKPH + MAPKpp -> MAPKppMAPKPH
a1 = 1.
RAF + RAFK -> RAFRAFK
a2 = 0.5
RAFp + RAFPH -> RAFpRAFPH
a3 = 3.3
MEK + RAFp -> MEKRAFp
a4 = 10.
MEKp + MEKPH -> MEKpMEKPH
a5 = 3.3
MEKp + RAFp -> MEKpRAFp
a6 = 10.
MEKPH + MEKpp -> MEKppMEKPH
a7 = 20.
MAPK + MEKpp -> MAPKMEKpp
a8 = 5.
MAPKp + MAPKPH -> MAPKpMAPKPH
a9 = 20.
MAPKp + MEKpp -> MAPKpMEKpp
d10 = 0.4
MAPKppMAPKPH -> MAPKPH + MAPKpp
d1 = 0.4
RAFRAFK -> RAF + RAFK
d2 = 0.5
RAFpRAFPH -> RAFp + RAFPH
d3 = 0.42
MEKRAFp -> MEK + RAFp
d4 = 0.8
MEKpMEKPH -> MEKp + MEKPH
d5 = 0.4
MEKpRAFp -> MEKp + RAFp
d6 = 0.8
MEKppMEKPH -> MEKPH + MEKpp
d7 = 0.6
MAPKMEKpp -> MAPK + MEKpp
d8 = 0.4
MAPKpMAPKPH -> MAPKp + MAPKPH
d9 = 0.6
MAPKpMEKpp -> MAPKp + MEKpp
k10 = 0.1
MAPKppMAPKPH -> MAPKp + MAPKPH
k1 = 0.1
RAFRAFK -> RAFK + RAFp
k2 = 0.1
RAFpRAFPH -> RAF + RAFPH
k3 = 0.1
MEKRAFp -> MEKp + RAFp
k4 = 0.1
MEKpMEKPH -> MEK + MEKPH
k5 = 0.1
MEKpRAFp -> MEKpp + RAFp
k6 = 0.1
MEKppMEKPH -> MEKp + MEKPH
k7 = 0.1
MAPKMEKpp -> MAPKp + MEKpp
k8 = 0.1
MAPKpMAPKPH -> MAPK + MAPKPH
k9 = 0.1
MAPKpMEKpp -> MAPKpp + MEKpp
Variable
IC
ODE
MAPK
0.3
MAPK'[t] == d7*MAPKMEKpp[t] + k8*MAPKpMAPKPH[t] -
a7*MAPK[t]*MEKpp[t]
MAPKMEKpp
0
MAPKMEKpp'[t] == -(d7*MAPKMEKpp[t]) - k7*MAPKMEKpp[t]
+ a7*MAPK[t]*MEKpp[t]
MAPKp
0
MAPKp'[t] == k7*MAPKMEKpp[t] - a8*MAPKp[t]*MAPKPH[t]
+ d8*MAPKpMAPKPH[t] + d9*MAPKpMEKpp[t] + k10*
MAPKppMAPKPH[t] - a9*MAPKp[t]*MEKpp[t]
MAPKPH
0.3
MAPKPH'[t] == -(a8*MAPKp[t]*MAPKPH[t]) + d8*MAPKpMAPKPH[
t] + k8*MAPKpMAPKPH[t] - a10*MAPKPH[t]*MAPKpp[t] +
d10*MAPKppMAPKPH[t] + k10*MAPKppMAPKPH[t]
MAPKpMAPKPH
0
MAPKpMAPKPH'[t] == a8*MAPKp[t]*MAPKPH[t] - d8*
MAPKpMAPKPH[t] - k8*MAPKpMAPKPH[t]
MAPKpMEKpp
0
MAPKpMEKpp'[t] == -(d9*MAPKpMEKpp[t]) - k9*MAPKpMEKpp[t]
+ a9*MAPKp[t]*MEKpp[t]
MAPKpp
0
MAPKpp'[t] == k9*MAPKpMEKpp[t] - a10*MAPKPH[t]*MAPKpp[t]
+ d10*MAPKppMAPKPH[t]
MAPKppMAPKPH
0
MAPKppMAPKPH'[t] == a10*MAPKPH[t]*MAPKpp[t] - d10*
MAPKppMAPKPH[t] - k10*MAPKppMAPKPH[t]
MEK
0.2
MEK'[t] == k4*MEKpMEKPH[t] + d3*MEKRAFp[t] -
a3*MEK[t]*RAFp[t]
MEKp
0
MEKp'[t] == -(a4*MEKp[t]*MEKPH[t]) + d4*MEKpMEKPH[t]
+ k6*MEKppMEKPH[t] + d5*MEKpRAFp[t] + k3*MEKRAFp[
t] - a5*MEKp[t]*RAFp[t]
MEKPH
0.2
MEKPH'[t] == -(a4*MEKp[t]*MEKPH[t]) + d4*MEKpMEKPH[t]
+ k4*MEKpMEKPH[t] - a6*MEKPH[t]*MEKpp[t] + d6*
MEKppMEKPH[t] + k6*MEKppMEKPH[t]
MEKpMEKPH
0
MEKpMEKPH'[t] == a4*MEKp[t]*MEKPH[t] - d4*MEKpMEKPH[t]
- k4*MEKpMEKPH[t]
MEKpp
0
MEKpp'[t] == d7*MAPKMEKpp[t] + k7*MAPKMEKpp[t] +
d9*MAPKpMEKpp[t] + k9*MAPKpMEKpp[t] - a7*MAPK[t]*
MEKpp[t] - a9*MAPKp[t]*MEKpp[t] - a6*MEKPH[t]*MEKpp[t]
+ d6*MEKppMEKPH[t] + k5*MEKpRAFp[t]
MEKppMEKPH
0
MEKppMEKPH'[t] == a6*MEKPH[t]*MEKpp[t] - d6*MEKppMEKPH[
t] - k6*MEKppMEKPH[t]
MEKpRAFp
0
MEKpRAFp'[t] == -(d5*MEKpRAFp[t]) - k5*MEKpRAFp[t]
+ a5*MEKp[t]*RAFp[t]
MEKRAFp
0
MEKRAFp'[t] == -(d3*MEKRAFp[t]) - k3*MEKRAFp[t] +
a3*MEK[t]*RAFp[t]
RAF
0.4
RAF'[t] == -(a1*RAF[t]*RAFK[t]) + k2*RAFpRAFPH[t] +
d1*RAFRAFK[t]
RAFK
0.1
RAFK'[t] == -(a1*RAF[t]*RAFK[t]) + d1*RAFRAFK[t] +
k1*RAFRAFK[t]
RAFp
0
RAFp'[t] == d5*MEKpRAFp[t] + k5*MEKpRAFp[t] +
d3*MEKRAFp[t] + k3*MEKRAFp[t] - a3*MEK[t]*RAFp[t]
- a5*MEKp[t]*RAFp[t] - a2*RAFp[t]*RAFPH[t] + d2*
RAFpRAFPH[t] + k1*RAFRAFK[t]
RAFPH
0.3
RAFPH'[t] == -(a2*RAFp[t]*RAFPH[t]) + d2*RAFpRAFPH[t]
+ k2*RAFpRAFPH[t]
RAFpRAFPH
0
RAFpRAFPH'[t] == a2*RAFp[t]*RAFPH[t] - d2*RAFpRAFPH[t]
- k2*RAFpRAFPH[t]
RAFRAFK
0
RAFRAFK'[t] == a1*RAF[t]*RAFK[t] - d1*RAFRAFK[t] -
k1*RAFRAFK[t]
Generated by Cellerator Version 1.4.3 (6-March-2004) using Mathematica 5.0
for Mac OS X (November 19, 2003), March 6, 2004 12:18:07, using (PowerMac,
PowerPC,Mac OS X,MacOSX,Darwin)
author=B.E.Shapiro
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2010 The BioModels.net Team.
For more information see the terms of use
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000011 | BioModels
Project description:Purpose: IGH sequencing has revolutionized analysis of structural and functional signatures of B cell clonality. The goals of this study are to compare IGH repertoire of splenic B cells before and after knockdown of long isoform of PRLR. Methods: After amplifying the IGH repertoire of splenic B cells using PCR primers for VHJ558 variable and Cμ constant regions. For next generation sequencing (NGS), a TrueSeq library was prepared by adapter ligation to full-length products and sequenced on the MiSeq Illumina 2x150 bp platform. Results: In this project, Unique nucleotide sequences were identified, their abundances were calculated, and their complementary determining region 3 (CDR3) length, CDR3 spectrum, VDJ usage, and diversity were analyzed using the International Immunogenetics Information System (IMGT) HighV-QUEST software. Controls are included C3,C4,C5,C7,C8 and C9. LFPRLR SMO treated mice samples are: A3,A4,A5,A6,A7 and A8
2023-03-06 | GSE207186 | GEO
Project description:The pontine noradrenergic cell groups, A5, A6 (locus coeruleus), and A7, provide the only noradrenergic innervation of the spinal cord, but the individual contribution of each of these populations to the regional innervation of the spinal cord remains controversial. We used an adeno-associated viral (AAV) vector encoding green fluorescent protein under an artificial dopamine beta-hydroxylase (PRSx8) promoter to trace the spinal projections from the A5, A6, and A7 groups. Projections from all three groups travel through the spinal cord in both the lateral and ventral funiculi and in the dorsal surface of the dorsal horn, but A6 axons take predominantly the dorsal and ventral routes, whereas A5 axons take mainly a lateral and A7 axons a ventral route. The A6 group provides the densest innervation at all levels, and includes all parts of the spinal gray matter, but it is particularly dense in the dorsal horn. The A7 group provides the next most dense innervation, again including all parts of the spinal cord, but is it denser in the ventral horn. The A5 group supplies only sparse innervation to the dorsal and ventral horns and to the cervical and lumbosacral levels, but provides the densest innervation to the thoracic intermediolateral cell column, and in particular to the sympathetic preganglionic neurons. Thus, the pontine noradrenergic cell groups project in a roughly topographic and complementary fashion onto the spinal cord. The pattern of spinal projections observed suggests that the locus coeruleus might have the greatest effect on somatosensory transmission, the A7 group on motor function, and the A5 group on sympathetic function.
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