ICGi022-A-1

SOD1-G128R_K7-4L-f, SOD1-G128R

General#

Cell Line

hPSCreg Name
ICGi022-A-1
Alternative name(s)
SOD1-G128R_K7-4L-f, SOD1-G128R
Cell line type Human induced pluripotent stem cell (hiPSC)
Last update 9th July 2021
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Provider

Generator The Federal Research Center Institute of Cytology and Genetics The Siberian Branch of the Russian Academy of Sciences (ICG)

External Databases

BioSamples SAMEA9333558
CLO CLO_0103475

General Information

* Is the cell line readily obtainable for third parties?
Yes
Research: allowed
Clinical: not allowed
Commercial: not allowed
Subclone of

Donor Information#

General Donor Information

Sex female
Ethnicity Caucasian

Phenotype and Disease related information (Donor)

Diseases No disease was diagnosed.
Disease associated phenotypes no phenotypes

Karyotyping (Donor)

Has the donor karyotype been analysed?
Unknown

Other Genotyping (Donor)

Is there genome-wide genotyping or functional data available?
Yes
Exome sequencing
https://www.ncbi.nlm.nih.gov/sra/?term=SRR11413027
No disease associated mutation found

External Databases (Donor)

BioSamples SAMN14446266

Ethics#

Also have a look at the ethics information for the parental line ICGi022-A .
Is there an MTA available for the cell line? No
For generation of the cell line, who was the supplier of any recombined DNA vectors or commercial kits used? IDT crRNA and tracrRNA were used for CRISPR/Cas9 gene editing
Are you aware of any constraints on the use or distribution of the cell line from the owner or any parties identified in the query above? No

hIPSC Derivation#

General

The source cell information can be found in the parental cell line ICGi022-A.
Passage number reprogrammed 1

Reprogramming method

Vector type Non-integrating
Vector Episomal
Genes
Is reprogramming vector detectable?
No
Methods used
PCR
Files and images showing reprogramming vector expressed or silenced

Vector free reprogramming

Type of used vector free reprogramming factor(s)
None

Other

Selection criteria for clones ESC-like morphology
Derived under xeno-free conditions
No
Derived under GMP?
No
Available as clinical grade?
No

Culture Conditions#

Surface coating Gelatin
Feeder cells Mouse embryonic fibroblasts
Cellfinder Ont Id: http://www.ebi.ac.uk/efo/EFO_0004040
Passage method Enzymatically
TrypLE
O2 Concentration 20 %
CO2 Concentration 5 %
Medium Other medium:
Base medium: Knock-out DMEM
Main protein source: Knock-out serum replacement
Serum concentration: 15 %
Supplements
GlutaMAX 2 mM
NEAA 0.1 mM
Penicillin-Streptomycin 100 U/ml
rhFGF basic 10 ng/ml
Has Rock inhibitor (Y27632) been used at passage previously with this cell line?
Yes
Has Rock inhibitor (Y27632) been used at cryo previously with this cell line?
No
Has Rock inhibitor (Y27632) been used at thaw previously with this cell line?
Yes

Characterisation#

Analysis of Undifferentiated Cells
Marker Expressed Immunostaining RT-PCR FACS Enzymatic Assay Expression Profiles
NANOG
Yes
SOX2
Yes
POU5F1 (OCT-4)
Yes
TRA 1-60
Yes
Score:
Marker Present Absent
mCpG
OCT4
Morphology pictures
Method documentation
Differentiation Potency
Endoderm
Ont Id: UBERON_0000925
In vitro spontaneous differentiation
Marker Expressed
KRT18
Yes
Morphology
Mesoderm
Ont Id: UBERON_0000926
In vitro spontaneous differentiation
Marker Expressed
ACTA2
Yes
Morphology
Neuron
Ont Id: CL_0000540
In vitro spontaneous differentiation
Marker Expressed
NEFH
Yes
Morphology

Microbiology / Virus Screening

Mycoplasma Negative

Genotyping#

Karyotyping (Cell Line)

Has the cell line karyotype been analysed?
Yes
46XX
Passage number: 15
Karyotyping method: G-Banding

Other Genotyping (Cell Line)

Genetic Modification#

Disease/phenotype related modifications
Amyotrophic Lateral Sclerosis
Synonyms
  • Amyotrophic Lateral Sclerosis
  • ALS
  • Lou Gehrig Disease
Genetic modifications
SOD1 (target)
Isogenic modification
21q22.11
NC_000021.9:c382G>C
NP_000445.1:pGly128Arg
Heterozygous
This mutation has been linked to ALS only once (PMID: 20192886) and has been described as highly severe with rapid progression, pain syndrome, and predominant lower motor neuron implication. It has been predicted bioinformatically that this substitution induces changes in the structure of the electrostatic loop, which binds copper ions essential for both stability and enzymatic activity of SOD1 protein
Mutated
G128R allele seq.png
Part of the SOD1 gene sequence of one of the alleles. Single nucleotide substitution, which leads to the amino acid substitution is present
Genetic modifications not related to a disease
SOD1 (target)
Isogenic modification
21q22.11
NC_000021.9:c385_386delinsTG
NP_000445.1:pLys129Ter
Heterozygous
The substitution of the two amino acids in the SOD1 gene was introduced as a result of CRISPR/Cas9-induced break repair. This substitution leads to the termination codon formation and, supposedly, translation of the truncated variant of SOD1 polypeptide.
Mutated
K129Ter allele seq.png
Part of the SOD1 gene sequence of one of the alleles. Two nucleotide substitution, which leads to the termination codon formation is present