School Of Basic And Applied Sciences
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Item Evolving strategies and application of proteins and peptide therapeutics in cancer treatment(Elsevier Masson s.r.l., 2023-05-05T00:00:00) Mukherjee, Anirban Goutam; Wanjari, Uddesh Ramesh; Gopalakrishnan, Abilash Valsala; Bradu, Pragya; Biswas, Antara; Ganesan, Raja; Renu, Kaviyarasi; Dey, Abhijit; Vellingiri, Balachandar; El Allali, Achraf; Alsamman, Alsamman M.; Zayed, Hatem; George Priya Doss, C.Several proteins and peptides have therapeutic potential and can be used for cancer therapy. By binding to cell surface receptors and other indicators uniquely linked with or overexpressed on tumors compared to healthy tissue, protein biologics enhance the active targeting of cancer cells, as opposed to the passive targeting of cells by conventional small-molecule chemotherapeutics. This study focuses on peptide medications that exist to slow or stop tumor growth and the spread of cancer, demonstrating the therapeutic potential of peptides in cancer treatment. As an alternative to standard chemotherapy, peptides that selectively kill cancer cells while sparing healthy tissue are developing. A mountain of clinical evidence supports the efficacy of peptide-based cancer vaccines. Since a single treatment technique may not be sufficient to produce favourable results in the fight against cancer, combination therapy is emerging as an effective option to generate synergistic benefits. One example of this new area is the use of anticancer peptides in combination with nonpeptidic cytotoxic drugs or the combination of immunotherapy with conventional therapies like radiation and chemotherapy. This review focuses on the different natural and synthetic peptides obtained and researched. Discoveries, manufacture, and modifications of peptide drugs, as well as their contemporary applications, are summarized in this review. We also discuss the benefits and difficulties of potential advances in therapeutic peptides. � 2023Item A Protein and Membrane Integrity Study of TiO2 Nanoparticles-Induced Mitochondrial Dysfunction and Prevention by Iron Incorporation(Springer, 2021-03-31T00:00:00) Barkhade, Tejal; Mahapatra, Santosh Kumar; Banerjee, IndraniThe paper assessed the toxic effect of titanium dioxide (TiO2) nanoparticles (NPs) on isolated mitochondria and its dysfunction prevention after Iron (Fe) incorporation. TiO2 and Fe content TiO2 NPs were synthesized and characterized using XPS, PL spectroscopy, and TEM. The nanostructure interaction with isolated mitochondria was investigated using circular dichroism (CD) confocal microscopy, flow cytometry, atomic force microscopy (AFM), surface-enhanced Raman spectroscopy (SERS), and FT-IR spectroscopy via nonspecific pathway. Fe content TiO2 NPs helps to control the dissolution rate of parent nanomaterial of TiO2 on the mitochondrial membrane. Confocal micrographs and flow cytometry results confirmed that Rhodamine 123 dye intensity get increased after interaction with Fe content TiO2 NPs which states the integrity of the mitochondrial membrane. AFM results revealed that TiO2 induces the swelling of mitochondrial tubules and also impaired the mitochondrial structure, whereas Fe content TiO2 NPs interaction prevents the impairment of mitochondrial tubules. The denaturation of a membrane protein by TiO2 interactions was observed through CD Spectroscopy. Further, nano-bio-interface study was performed using SERS, through shifting and extinct of peaks affiliated to membrane proteins and lipids. However, Fe content TiO2-treated samples showed a significant increase in the membrane potential of mitochondria via flow cytometry results. Graphic Abstract: [Figure not available: see fulltext.] � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Effect of degree of milling on physicochemical, structural, pasting and cooking properties of short and long grain Indica rice cultivars(Elsevier Ltd, 2018) Sandhu, Rubrinder Singh; Singh, Narpinder; Kaler, R.S.S.; Kaur, Amritpal; Shevkani, KhetanThe effects of degree of milling (DOM) between 0 and 8% on physico-chemical, structural, pasting and cooking properties of short and long grain Indica rice cultivars were studied. Ash, protein, lipids and minerals decreased while blue value and crystallinity increased with increase in DOM. The colour parameters (a? b?) and cooking time (CT) decreased while L?(lightness) increased with increase in DOM. Elongation ratio (ER), gruel solid loss (GSL), length/breadth (L/B) and paste viscosities during cooking increased with increase in DOM. Short grain rice contained lower ash, protein, lipids, Mn, K, Ca, CT and GSL than long grain while the later showed higher crystallinity, Mn, P, K, Ca and ER. Paste and dough characteristics measured using Rheometer and Mixolab, respectively correlated well and differed with cultivar and DOM. Short and long grain cultivars showed variation in loss of different chemical constituents during varied DOM causing variation in cooking characteristics. ? 2018 Elsevier LtdItem Stage-specific functions of Semaphorin7A during adult hippocampal neurogenesis rely on distinct receptors(Nature Publishing Group, 2017) Jongbloets, Bart C.; Lemstra, Suzanne; Schellino, Roberta; Broekhoven, Mark H.; Parkash, Jyoti; Hellemons, Anita J.C.G.M.; Mao, Tianyi; Giocobini, Paolo; Praag, Henriette Van; Marchis, Silvia De; Ramakers, Geert M.J.; Pasterkamp, R. Jeroen; Jongbloets, B.C.; Lemstra, S.; Schellino, R.; Broekhoven, M.H.; Parkash, J.; Hellemons, A.J.C.G.M.; Mao, T.; Giacobini, P.; Van Praag, H.; De Marchis, S.; Ramakers, G.M.J.; Pasterkamp, R.J.The guidance protein Semaphorin7A (Sema7A) is required for the proper development of the immune and nervous systems. Despite strong expression in the mature brain, the role of Sema7A in the adult remains poorly defined. Here we show that Sema7A utilizes different cell surface receptors to control the proliferation and differentiation of neural progenitors in the adult hippocampal dentate gyrus (DG), one of the select regions of the mature brain where neurogenesis occurs. PlexinC1 is selectively expressed in early neural progenitors in the adult mouse DG and mediates the inhibitory effects of Sema7A on progenitor proliferation. Subsequently, during differentiation of adult-born DG granule cells, Sema7A promotes dendrite growth, complexity and spine development through ?1-subunit-containing integrin receptors. Our data identify Sema7A as a key regulator of adult hippocampal neurogenesis, providing an example of how differential receptor usage spatiotemporally controls and diversifies the effects of guidance cues in the adult brain.Item Elevated level of acetylation of APE1 in tumor cells modulates DNA damage repair(Impact Journals LLC, 2016) Sengupta, S.; Mantha, Anil K.; Song, H.; Roychoudhury, S.; Nath, S.; Ray, S.; Bhakat, K.K.Apurinic/apyrimidinic (AP) sites are frequently generated in the genome by spontaneous depurination/depyrimidination or after removal of oxidized/modified bases by DNA glycosylases during the base excision repair (BER) pathway. Unrepaired AP sites are mutagenic and block DNA replication and transcription. The primary enzyme to repair AP sites in mammalian cells is AP endonuclease (APE1), which plays a key role in this repair pathway. Although overexpression of APE1 in diverse cancer types and its association with chemotherapeutic resistance are well documented, alteration of posttranslational modification of APE1 and modulation of its functions during tumorigenesis are largely unknown. Here, we show that both classical histone deacetylase HDAC1 and NAD+-dependent deacetylase SIRT1 regulate acetylation level of APE1 and acetylation of APE1 enhances its AP-endonuclease activity both in vitro and in cells. Modulation of APE1 acetylation level in cells alters AP site repair capacity of the cell extracts in vitro. Primary tumor tissues of diverse cancer types have higher level of acetylated APE1 (AcAPE1) compared to adjacent non-tumor tissue and exhibit enhanced AP site repair capacity. Importantly, in the absence of APE1 acetylation, cells accumulate AP sites in the genome and show increased sensitivity to DNA damaging agents. Together, our study demonstrates that elevation of acetylation level of APE1 in tumor could be a novel mechanism by which cells handle the elevated levels of DNA damages in response to genotoxic stress and maintain sustained proliferation.