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Malini Varadarajan

Researcher at Massachusetts Institute of Technology

Publications -  9
Citations -  1348

Malini Varadarajan is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Gene & Insertional mutagenesis. The author has an hindex of 7, co-authored 8 publications receiving 1235 citations.

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Haploid Genetic Screens in Human Cells Identify Host Factors Used by Pathogens

TL;DR: Using insertional mutagenesis to develop a screening method to generate null alleles in a human cell line haploid for all chromosomes except chromosome 8, host factors essential for infection with influenza and genes encoding important elements of the biosynthetic pathway of diphthamide, which are required for the cytotoxic effects ofdiphtheria toxin and exotoxin A are identified.
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Generation of iPSCs from cultured human malignant cells.

TL;DR: The generation and characterization of iPSCs derived from human chronic myeloid leukemia cells are described and it is shown that, despite the presence of oncogenic mutations, these cells acquired pluripotency by the expression of 4 transcription factors and underwent differentiation into cell types derived of all 3 germ layers during teratoma formation.
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Global gene disruption in human cells to assign genes to phenotypes by deep sequencing

TL;DR: This work uses a retroviral gene-trap vector to generate insertions in >98% of the genes expressed in a human cancer cell line that is haploid for all but one of its chromosomes to identify 743 mutations distributed over 12 human genes important for intoxication by four different CDTs.

Global gene disruption in human cells to assign genes to phenotypes

TL;DR: Ploegh et al. as mentioned in this paper developed a mutagenesis-based screening approach in human cells using insertional mutagenisation in KBM7 cells, a chronic myeloid leukemia cell line that is haploid for all chromosomes except chromosome 81.
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A haploid genetic screen identifies the major facilitator domain containing 2A (MFSD2A) transporter as a key mediator in the response to tunicamycin

TL;DR: A critical role is uncovered for MFSD2A by acting as a putative TM transporter at the plasma membrane by identifying transmembrane helical amino acid residues essential for mediating TM sensitivity.