Search Results - "Kadamb, Rama"

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  1. 1

    Invasive phenotype in triple negative breast cancer is inhibited by blocking SIN3A–PF1 interaction through KLF9 mediated repression of ITGA6 and ITGB1 by Kadamb, Rama, Leibovitch, Boris A, Farias, Eduardo F, Dahiya, Nisha, Suryawanshi, Hemant, Bansal, Nidhi, Waxman, Samuel

    Published in Translational oncology (01-02-2022)
    “…•We show that the PAH2 domain of SIN3A is a target when it is inhibited from binding to PF1 results in inhibition of invasive phenotype in TNBC.•Epigenetic…”
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  2. 2

    The Sin3A/MAD1 Complex, through Its PAH2 Domain, Acts as a Second Repressor of Retinoic Acid Receptor Beta Expression in Breast Cancer Cells by Dahiya, Nisha Rani, Leibovitch, Boris A, Kadamb, Rama, Bansal, Nidhi, Waxman, Samuel

    Published in Cells (Basel, Switzerland) (31-03-2022)
    “…Retinoids are essential in balancing proliferation, differentiation and apoptosis, and they exert their effects through retinoic acid receptors (RARs) and…”
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  3. 3

    Tumor suppressor protein p53 recruits human Sin3B/HDAC1 complex for down-regulation of its target promoters in response to genotoxic stress by Bansal, Nidhi, Kadamb, Rama, Mittal, Shilpi, Vig, Leena, Sharma, Raisha, Dwarakanath, Bilikere S, Saluja, Daman

    Published in PloS one (20-10-2011)
    “…Master regulator protein p53, popularly known as the "guardian of genome" is the hub for regulation of diverse cellular pathways. Depending on the cell type…”
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  4. 4

    Sin3: Insight into its transcription regulatory functions by Kadamb, Rama, Mittal, Shilpi, Bansal, Nidhi, Batra, Harish, Saluja, Daman

    Published in European journal of cell biology (01-08-2013)
    “…Sin3, a large acidic protein, shares structural similarity with the helix-loop-helix dimerization domain of proteins of the Myc family of transcription…”
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  5. 5
  6. 6

    Abstract 31: Targeted dissociation of PF1 from SIN3A chromatin regulator complex inhibits tumor growth and metastasis in triple-negative breast cancer by Kadamb, Rama, Bansal, Nidhi, Leibovitch, Boris A, Kwon, Yeon-Jin, Zhou, Ming-Ming, Farias, Eduardo, Waxman, Samuel

    Published in Cancer research (Chicago, Ill.) (01-07-2018)
    “…Abstract Triple negative breast cancer (TNBC) is characterized by an aggressive, poorly differentiated phenotype associated with early recurrence. Chemotherapy…”
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  7. 7

    Abstract A009: NR2F1 inhibits Gaq/11-YAP-TAZ signaling and limits reactivation of uveal melanoma disseminated cancer cells via induction of dormancy by Kadamb, Rama, Anton, Melisa Lopez, Chua, Vivian, Purwin, Timothy, Toledano, Maria Angelo Nieto, Aplin, Andrew, Aguirre-Ghiso, Julio

    Published in Cancer research (Chicago, Ill.) (15-01-2023)
    “…Abstract Introduction: At the time of diagnosis, less than 5% of uveal melanoma (UM) patients have evidence of metastasis. However, up to 50% of UM patients…”
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  8. 8

    Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes by Kadamb, Rama, Mittal, Shilpi, Bansal, Nidhi, Saluja, Daman

    Published in Bioscience reports (01-08-2015)
    “…The multiprotein SWI-independent 3 (Sin3)-HDAC (histone deacetylase) corepressor complex mediates gene repression through its interaction with DNA-binding…”
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  9. 9

    Abstract 747: p53 activation through stress induction mediates differential regulation of target genes by Mittal, Shilpi, Kadamb, Rama, Bansal, Nidhi, Saluja, Daman

    Published in Cancer research (Chicago, Ill.) (15-04-2013)
    “…Abstract p53 is a sequence specific transcription factor that gets up regulated in response to stress such as DNA damage, microtubule disruption or oxidative…”
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  10. 10

    Abstract 748: Studying the significance of human p53-Sin3B interaction under the condition of DNA damage by Kadamb, Rama, Mittal, Shilpi, Bansal, Nidhi, Dwarakanath, Bilikere Srinivasa Rao, Saluja, Daman

    Published in Cancer research (Chicago, Ill.) (15-04-2013)
    “…Abstract Sin3, a global regulator of transcription plays an important role in mediating gene regulation, by binding to various transcription factors through…”
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