Anindya Sen

Anindya Sen

Cambridge, Massachusetts, United States
7K followers 500+ connections

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About

Neuroscientist, with 12+ years of scientific and managerial experience. My overarching…

Activity

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Experience

  • Crane Biosciences Inc. Graphic

    Crane Biosciences Inc.

    London Area, United Kingdom

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    Cambridge, Massachusetts, United States

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    New York City Metropolitan Area

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    New York City Metropolitan Area

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    New York, United States

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    Greater New York City Area

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    Cambridge

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    Cambridge, MA

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    Cambridge, MA

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    Cambridge, MA

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    Greater Boston Area

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    Greater New York City Area

Education

Volunteer Experience

  • The Lesbian, Gay, Bisexual and Transgender Community Center Graphic

    Library volunteer

    The Lesbian, Gay, Bisexual and Transgender Community Center

    - 2 years 4 months

    Human Rights

    https://gaycenter.org/about

  • MASALA executive committee

    MASALA: Boston based South Asian LGBTQ+ organizaton

    - 2 years 1 month

    Human Rights

    Massachusetts Area South Asian Lambda Association (MASALA) is a social group based in Boston, that provides a safe and supportive environment to New England based Gay, Lesbian, Bi, Trans, and Questioning South Asians (people from Afghanistan, Bangladesh, Bhutan, Burma, India, Iran, Maldives, Nepal, Pakistan, Sri Lanka, and Tibet; and from the global South Asian Diaspora).

    MASALA is an avenue where distinctions of social class, status, religious affiliations and regional identities…

    Massachusetts Area South Asian Lambda Association (MASALA) is a social group based in Boston, that provides a safe and supportive environment to New England based Gay, Lesbian, Bi, Trans, and Questioning South Asians (people from Afghanistan, Bangladesh, Bhutan, Burma, India, Iran, Maldives, Nepal, Pakistan, Sri Lanka, and Tibet; and from the global South Asian Diaspora).

    MASALA is an avenue where distinctions of social class, status, religious affiliations and regional identities dissolve while cultural richness, linguistic diversity and individuality are maintained to inform, enrich and empower.

  • Harvard Medical School Graphic

    Postdoctoral Researcher

    Harvard Medical School

    - 4 years

    Health

Publications

  • Genetic circuitry modulating notch signals through endosomal trafficking.

    Methods Enzymol.

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  • Genetic circuitry of Survival motor neuron, the gene underlying spinal muscular atrophy

    Proc Natl Acad Sci

    The clinical severity of the neurodegenerative disorder spinal muscular atrophy (SMA) is dependent on the levels of functional Survival Motor Neuron (SMN) protein. Consequently, current strategies for developing treatments for SMA generally focus on augmenting SMN levels. To identify additional potential therapeutic avenues and achieve a greater understanding of SMN, we applied in vivo, in vitro, and in silico approaches to identify genetic and biochemical interactors of the Drosophila SMN…

    The clinical severity of the neurodegenerative disorder spinal muscular atrophy (SMA) is dependent on the levels of functional Survival Motor Neuron (SMN) protein. Consequently, current strategies for developing treatments for SMA generally focus on augmenting SMN levels. To identify additional potential therapeutic avenues and achieve a greater understanding of SMN, we applied in vivo, in vitro, and in silico approaches to identify genetic and biochemical interactors of the Drosophila SMN homolog. We identified more than 300 candidate genes that alter an Smn-dependent phenotype in vivo. Integrating the results from our genetic screens, large-scale protein interaction studies, and bioinformatic analysis, we define a unique interactome for SMN that provides a knowledge base for a better understanding of SMA

    Other authors
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  • Notch signaling at a glance.

    J Cell Sci.

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  • An extracellular region of Serrate is essential for ligand-induced cis-inhibition of Notch signaling.

    Development. 2013 May;140(9):2039-49. doi: 10.1242/dev.087916.

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  • Regulation of ligand-independent Notch signal through intracellular trafficking.

    Commun Integr Biol.

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  • Synergy between the ESCRT-III complex and Deltex defines a ligand-independent Notch signal.

    J Cell Biol. 2011

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  • Modeling spinal muscular atrophy in Drosophila links Smn to FGF signaling.

    J Cell Biol.

    Spinal muscular atrophy (SMA), a devastating neurodegenerative disorder characterized by motor neuron loss and muscle atrophy, has been linked to mutations in the Survival Motor Neuron (SMN) gene. Based on an SMA model we developed in Drosophila, which displays features that are analogous to the human pathology and vertebrate SMA models, we functionally linked the fibroblast growth factor (FGF) signaling pathway to the Drosophila homologue of SMN, Smn. Here, we characterize this relationship…

    Spinal muscular atrophy (SMA), a devastating neurodegenerative disorder characterized by motor neuron loss and muscle atrophy, has been linked to mutations in the Survival Motor Neuron (SMN) gene. Based on an SMA model we developed in Drosophila, which displays features that are analogous to the human pathology and vertebrate SMA models, we functionally linked the fibroblast growth factor (FGF) signaling pathway to the Drosophila homologue of SMN, Smn. Here, we characterize this relationship and demonstrate that Smn activity regulates the expression of FGF signaling components and thus FGF signaling. Furthermore, we show that alterations in FGF signaling activity are able to modify the neuromuscular junction defects caused by loss of Smn function and that muscle-specific activation of FGF is sufficient to rescue Smn-associated abnormalities

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  • Conserved genes act as modifiers of invertebrate SMN loss of function defects.

    PLoS Genetics

    Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular…

    Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular defects. To find genes that modulate SMN function defects across species, two approaches were used. First, a genome-wide RNAi screen for C. elegans SMN modifier genes was undertaken, yielding four genes. Second, we tested the conservation of modifier gene function across species; genes identified in one invertebrate model were tested for function in the other invertebrate model. Drosophila orthologs of two genes, which were identified originally in C. elegans, modified Drosophila SMN loss of function defects. C. elegans orthologs of twelve genes, which were originally identified in a previous Drosophila screen, modified C. elegans SMN loss of function defects. Bioinformatic analysis of the conserved, cross-species, modifier genes suggests that conserved cellular pathways, specifically endocytosis and mRNA regulation, act as critical genetic modifiers of SMN loss of function defects across species.

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  • Modeling spinal muscular atrophy in Drosophila.

    PLoS One

    Spinal Muscular Atrophy (SMA), a recessive hereditary neurodegenerative disease in humans, has been linked to mutations in the survival motor neuron (SMN) gene. SMA patients display early onset lethality coupled with motor neuron loss and skeletal muscle atrophy. We used Drosophila, which encodes a single SMN ortholog, survival motor neuron (Smn), to model SMA, since reduction of Smn function leads to defects that mimic the SMA pathology in humans. Here we show that a normal neuromuscular…

    Spinal Muscular Atrophy (SMA), a recessive hereditary neurodegenerative disease in humans, has been linked to mutations in the survival motor neuron (SMN) gene. SMA patients display early onset lethality coupled with motor neuron loss and skeletal muscle atrophy. We used Drosophila, which encodes a single SMN ortholog, survival motor neuron (Smn), to model SMA, since reduction of Smn function leads to defects that mimic the SMA pathology in humans. Here we show that a normal neuromuscular junction (NMJ) structure depends on SMN expression and that SMN concentrates in the post-synaptic NMJ regions. We conducted a screen for genetic modifiers of an Smn phenotype using the Exelixis collection of transposon-induced mutations, which affects approximately 50% of the Drosophila genome. This screen resulted in the recovery of 27 modifiers, thereby expanding the genetic circuitry of Smn to include several genes not previously known to be associated with this locus. Among the identified modifiers was wishful thinking (wit), a type II BMP receptor, which was shown to alter the Smn NMJ phenotype. Further characterization of two additional members of the BMP signaling pathway, Mothers against dpp (Mad) and Daughters against dpp (Dad), also modify the Smn NMJ phenotype. The NMJ defects caused by loss of Smn function can be ameliorated by increasing BMP signals, suggesting that increased BMP activity in SMA patients may help to alleviate symptoms of the disease. These results confirm that our genetic approach is likely to identify bona fide modulators of SMN activity, especially regarding its role at the neuromuscular junction, and as a consequence, may identify putative SMA therapeutic targets

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  • Distinct types of glial cells populate the Drosophila antenna.

    BMC Dev Biol

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Honors & Awards

  • Teaching Award

    Harvard University Undergraduate Education

    Teaching Award for LS1A and LS1B, 2009-2013

  • Post Doctoral Fellowship: Modifiers of SMN Using Transgenic Drosophila as a Model System

    Families of Spinal Muscular Atrophy (FSMA)

    Background: Spinal Muscular Atrophy is an autosomal recessive neurodegenerative disease that is the leading cause of genetically-linked infant mortality. The observation of fundamental importance with respect to developing treatments for SMA is that the severity of the disease relies critically on the amount of Survival Motor Neuron (SMN) protein present in the affected individual.

    Anticipated Results: We will identify different factors that regulate SMN with an aim to find new…

    Background: Spinal Muscular Atrophy is an autosomal recessive neurodegenerative disease that is the leading cause of genetically-linked infant mortality. The observation of fundamental importance with respect to developing treatments for SMA is that the severity of the disease relies critically on the amount of Survival Motor Neuron (SMN) protein present in the affected individual.

    Anticipated Results: We will identify different factors that regulate SMN with an aim to find new therapeutic strategies for SMA by identifying novel drug targets.

    http://www.fsma.org/Researchers/BasicResearchFundingOpportunities/AwardedGrants/2009/index.cfm?dspPrintReady=Y

  • Kanwal Rekhi Career Development Fellowships

    TIFR

  • Boehringer–Ingelheim Fonds Travel Grant

    Boehringer–Ingelheim Fonds

    http://www.bifonds.de/fellowships-grants/travel-grants.html

  • Company of Biologists Fellowship

    Company of Biologists

    http://dev.biologists.org/site/misc/fellowships.xhtml

  • Financial Aid award

    Marine Biological Laboratory

    Financial Aid award from Marine Biological Laboratory to attend Embryology course (June 2001)

    http://hermes.mbl.edu/education/courses/summer/course_embryo.html

  • Wood-Whelan Fellowship 2001

    International Union of Biochemistry and Molecular Biology

    Mechanisms determining cell fate choice in the Drosophila olfactory system (4 months)
    http://www.iubmb.org/index.php?id=118

  • President's Gold Medal

    Govt. of India

  • National Scholarship

    Govt. Of India for B.Sc.

  • Biotechnology Master's Fellowship

    Department of Biotechnology (DBT)

Languages

  • English

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  • Hindi

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  • Bengali

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