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STBCi004-B-1

SFC832-03-06 LRRK2WT/WT C47

Gene-edited iPSC line

Immediately available for distribution*
*Once all legal and processing details completed
Timepoint: confluency
Magnification: 4x
Timepoint: confluency
Magnification: 10x
A CLIP contains information about a cell line including any specific third party obligations relating to, for example, licensing obligations or the donor consent which affect the use of the cell line.

The EBiSC Access and Use Agreement must be completed along with an individual Cell Line Information Pack for each line. Complete the EAUA and send to Contact@EBiSC.org for countersignature. The EAUA must be fully signed before proceeding with your order.
A batch specific Certificate of Analysis will be available to download once you receive your EBiSC iPSC line.

General#

Cell Line

hPSCreg name STBCi004-B-1
Alternative name(s)
SFC832-03-06 LRRK2WT/WT C47
Cell line type Human induced pluripotent stem cell (hiPSC)
Similar lines
STBCi004-B
(SFC832-03-06)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi004-A
(SFC832-03-19)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi004-C
(SFC832-03-07)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi005-A
(SFC833-03-01)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi007-A
(SFC855-03-06)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi007-A
(MK002-4)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi008-B
(MK144-7)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi007-B
(MK002-6)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi007-C
(MK002-7)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi008-A
(MK144-1)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
UOXFi008-C
(MK144-10)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
ESi006-A
(SP13#4)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi005-B
(SFC833-03-05)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi005-C
(SFC833-03-14)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi007-B
(SFC855-03-08)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi007-C
(SFC855-03-01)
Donor's gene variants:
LRRK2
Donor diseases:
Parkinson disease
STBCi026-A-1
(SFC840-03-03 LRRK2-/-D10)
STBCi026-A-3
(SFC840-03-03 LRRK2 WT/R1441C H3)
STBCi026-A-2
(SFC840-03-03 LRRK2-/-C11)
EDi001-A-1
(AST22-C, AST23-C)
Donor's gene variants:
SNCA, SNCA
Donor diseases:
Parkinson disease
EDi001-A-2
(AST23-1KO-3, AST22-1KO-3, AST-23_SCAKO Clone 3, AST-22_SNCAKO Clone 3)
Donor's gene variants:
SNCA, SNCA, SNCA, SNCA
Donor diseases:
Parkinson disease
EDi001-A-3
(AST23_SNCAKO Clone 1, AST22-1KO-1, AST23-1KO-1, AST22_SNCAKO Clone 1)
Donor's gene variants:
SNCA, SNCA, SNCA, SNCA
Donor diseases:
Parkinson disease

Provider

Depositor StemBANCC (STBC)
Distributors
EBiSC

External Databases

hPSCreg STBCi004-B-1
BioSamples SAMEA5859478
Cellosaurus CVCL_A8X1
Wikidata Q102114943

General Information

Publications View all related publications on hPSCreg (1)
This EBiSC line can be used for:
Yes
Research use: allowed
Clinical use: no
Commercial use: no
Subclone of

Donor Information#

General Donor Information

Sex female

Phenotype and Disease related information (Donor)

Diseases A disease was diagnosed.
The donor is a carrier of a disease-associated mutation and affected.
Synonyms
  • Parkinson disease
  • Parkinson's disease
  • paralysis agitans
Genetic variants
LRRK2 (target)
12q12
NM_198578.3:c.6055G>A
NP_940980.3:p.Gly2019Ser
LRRK2 G2019S

Donor Relations

Other cell lines of this donor

External Databases (Donor)

BioSamples SAMEA104129730

hIPSC Derivation#

General

The source cell information can be found in the parental cell line STBCi004-B.

Reprogramming method

Vector type Non-integrating
Vector Sendai virus
Genes
Is reprogramming vector detectable?
No
Methods used
PCR

Vector free reprogramming

Other

Derived under xeno-free conditions
Unknown
Derived under GMP?
Unknown
Available as clinical grade?
Unknown

Culture Conditions#

Latest released batch

Culture medium mTeSR1
Passage method EDTA
Surface coating Matrigel
O2 concentration 21
CO2 concentration 5
Temperature 37 °C
The following are the depositor culture conditions, they do not refer to any specific batch.
Surface coating Matrigel/Geltrex
Feeder cells
No
Passage method Enzyme-free cell dissociation
EDTA
Medium mTeSR™ 1

Characterisation#

Analysis of Undifferentiated Cells
Marker Expressed Immunostaining RT-PCR Flow Cytometry Enzymatic Assay Expression Profiles
NANOG
Yes
TRA 1-60
Yes
POU5F1 (OCT-4)
Yes
SSEA-4
Yes
Spontaneous EB differentiation and qPCR for trilineage markers
Differentiation Potency
Endoderm
Ont Id: UBERON_0000925
In vitro spontaneous differentiation
Marker Expressed
CXCR4
Yes
GATA6
Yes
SOX17
Yes
Mesoderm
Ont Id: UBERON_0000926
In vitro spontaneous differentiation
Marker Expressed
VIM
Yes
DCN
Yes
MLX1
Yes
Ectoderm
Ont Id: UBERON_0000924
In vitro spontaneous differentiation
Marker Expressed
HES5
Yes
NEUROD1
Yes
PAX6
Yes

Microbiology / Virus Screening

HIV 1 Negative
HIV 2 Negative
Hepatitis B Negative
Hepatitis C Negative
Mycoplasma Negative

Sterility

Inoculation for microbiological growth No Contaminants Detected
Mycoplasma Not Detected
Viability Viable post-cryopreservation

Genotyping#

Karyotyping (Cell Line)

Has the cell line karyotype been analysed?
Yes
Karyotype abnormalities: none compared to fibroblasts
Passage number: 40
Karyotyping method: Molecular karyotyping by SNP array
http://

Other Genotyping (Cell Line)

Genetic Modification#

Disease/phenotype related modifications
Synonyms
  • Parkinson disease
  • Parkinson's disease
  • paralysis agitans
Genetic modifications
LRRK2 (target)
Isogenic modification
12q12
The G2019S variant (NM_198578.3:c.6055G>A) in the gene LRRK2 was normalized by gene editing, resulting in the wt form: NM_198578.3:c.6055G. CRISPR/Cas9-mediated double-strand break generated close to G2019S mutation and homology-directed repair with donor sequence. Homology arms generated by amplification of LRRK2 sequence in mutant allele to maintain isogeneic sequence. The G2019S mutation was repaired (G>A), and other silent mutations introduced including mutated protospacer adjacent motifs to prevent recutting of repaired sequence, and a PstI site for identification of repaired clones. See Certificate of Analysis.
Repaired