CUIMCi004-A-2

1514_1 #1 CL3

The cell line is not validated yet.

General

Cell Line

hPSCreg name CUIMCi004-A-2
Cite as:
CUIMCi004-A-2
Alternative name(s)
1514_1 #1 CL3
Cell line type Human induced pluripotent stem cell (hiPSC)
Similar lines No similar lines found.
Last update 1st November 2025
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Provider

Generator Columbia University Irving Medical Center (CUIMC)
Owner Columbia University Irving Medical Center (CUIMC)
Distributors
Derivation country United States

General Information

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

Donor Information

General Donor Information

Sex male
Ethnicity Non Hispanic White

Phenotype and Disease related information (Donor)

Diseases A disease was diagnosed.
Synonyms
  • Severe_Obesity
  • Class 3 Obesity
  • Severe Obesity
  • Extreme Obesity
  • Class III Obesity
show more synonyms

Other Genotyping (Donor)

Is there genome-wide genotyping or functional data available?
No

Donor Relations

Other cell lines of this donor

External Databases (Donor)

BioSamples SAMEA12576724

Ethics

Also have a look at the ethics information for the parental line CUIMCi004-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?

hIPSC Derivation

General

The source cell information can be found in the parental cell line CUIMCi004-A.

Reprogramming method

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

Vector free reprogramming

Other

Selection criteria for clones Clones were manually picked according to their morphology, then characterized for pluripotency, stemness, and others
Derived under xeno-free conditions
No
Derived under GMP?
No
Available as clinical grade?
No

Culture Conditions

Surface coating Matrigel/Geltrex
Feeder cells
No
Passage method Enzyme-free cell dissociation
EDTA
O2 Concentration 20 %
CO2 Concentration 5 %
Medium mTeSR™ Plus
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?
Yes
Has Rock inhibitor (Y27632) been used at thaw previously with this cell line?
Yes

Characterisation

Analysis of Undifferentiated Cells
Marker Expressed Immunostaining RT-PCR Flow Cytometry Enzymatic Assay Expression Profiles
NANOG
Yes
POU5F1 (OCT-4)
Yes
SOX2
Yes
Differentiation Potency
Endoderm
Ont Id: NCIT_C12706
In vitro directed differentiation
Marker Expressed
Sox17
Yes
Morphology
Protocol or reference
Mesoderm
Ont Id: UBERON_0000926
In vitro directed differentiation
Marker Expressed
Bry (T)
Yes
Morphology
Protocol or reference
Ectoderm
Ont Id: UBERON_0000924
In vitro directed differentiation
Marker Expressed
Otx2
Yes
Otx2
Unknown
Morphology
Protocol or reference

Microbiology / Virus Screening

Mycoplasma Negative

Genotyping

Karyotyping (Cell Line)

Has the cell line karyotype been analysed?
Yes
46XY
Passage number: p26
Karyotyping method: G-Banding

Other Genotyping (Cell Line)

Genetic Modification

Disease/phenotype related modifications
The parental cell line CUIMCi004-A was derived from a patient with severe early-onset obesity and carries a frameshift variant in a hemizygous state (c.2136_2139del + 1insCT). CUIMCi004-A-1 is a subclone of this parental line, in which the frameshift variant has been corrected.
Synonyms
  • Severe_Obesity
  • Class 3 Obesity
  • Severe Obesity
  • Extreme Obesity
  • Class III Obesity
show more synonyms
Genetic modifications
Isogenic modification
Chromosome X: 129,539,849-129,592,561
NM_000276.4: c.2136_2139del + 1insCT
NP_000267.2 :p.(L713Rfs*28)
hemizygous
A CRISPR-Cas9 approach, following our previously published protocol (https://pubmed.ncbi.nlm.nih.gov/35950852/ ), was used to correct the frameshift variant in the patient-derived iPSC line (CUIMCi004-A). Sanger sequencing was performed to confirm the presence of the frameshift variant in the parental cell line and, after gene editing, to screen for corrected clones. The absence of the variant in one subclone, as confirmed by Sanger sequencing, validated the successful correction of the mutation.
Repaired