Search

Your search keyword '"Shrabastee Chakraborty"' showing total 5 results
Start Over Author "Shrabastee Chakraborty"
5 results on '"Shrabastee Chakraborty"'

1. Tumor Suppressors Having Oncogenic Functions: The Double Agents

Author

Neerajana Datta, Shrabastee Chakraborty, Malini Basu, and Mrinal K. Ghosh

Subjects
tumor suppressor genes, Rb, PTEN, FOXO, PML, cancer, Cytology, QH573-671
Abstract

Cancer progression involves multiple genetic and epigenetic events, which involve gain-of-functions of oncogenes and loss-of-functions of tumor suppressor genes. Classical tumor suppressor genes are recessive in nature, anti-proliferative, and frequently found inactivated or mutated in cancers. However, extensive research over the last few years have elucidated that certain tumor suppressor genes do not conform to these standard definitions and might act as “double agents”, playing contrasting roles in vivo in cells, where either due to haploinsufficiency, epigenetic hypermethylation, or due to involvement with multiple genetic and oncogenic events, they play an enhanced proliferative role and facilitate the pathogenesis of cancer. This review discusses and highlights some of these exceptions; the genetic events, cellular contexts, and mechanisms by which four important tumor suppressors—pRb, PTEN, FOXO, and PML display their oncogenic potentials and pro-survival traits in cancer. more...

Published
2020
Full Text
View/download PDF

2. E3 Ubiquitin Ligase CHIP Drives Monoubiquitination-mediated Nuclear Import of Tumor Suppressor PTEN

Author

Shrabastee Chakraborty, Subhajit Karmakar, Malini Basu, and Mrinal K. Ghosh

Abstract

Nuclear localization of Phosphatase and Tensin Homolog Deleted on Chromosome TEN (PTEN) is crucial for its tumor suppressive activities. Monoubiquitination has been established as a principal mechanism driving nuclear translocation of PTEN. In this study, we describe a novel mechanism wherein Carboxy terminus of Hsc70 Interacting Protein (CHIP) mediates monoubiquitination of PTEN, leading to the latter’s nuclear import. Analysis of subcellular fractions of multiple cell lines revealed a rise in both nuclear and total cellular PTEN levels under monoubiquitination-promoting conditions, an effect that was abrogated when CHIP expression was silenced. We established a time-point kinetics of CHIP-mediated nuclear translocation of PTEN using immunocytochemistry. We identified a role of Karyopherin α1 (KPNA1) in facilitating nuclear transport of monoubiquitinated PTEN. We further established a direct interaction between CHIP and PTEN inside the nuclear compartment, where CHIP could participate in either polyubiquitination or monoubiquitination of the latter. CHIP was found to monoubiquitinate PTEN on K13 and K289 residues. Finally, we showed that CHIP-mediated monoubiquitination of PTEN resulted in increased apoptosis, decreased cell viability and proliferation. This enhancement of PTEN’s tumor suppressive abilities by CHIP involved modulation of transcriptional activities of PTEN. To the best of our knowledge, this is the first report elucidating CHIP’s non-canonical roles on PTEN, which is also established here as a nuclear interacting partner of CHIP. more...

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results

3. Contributors

Author

Krishnendu Adhikary, Brenda Affinati, Amany M. Ahmed, Mahmoud Al Saadi, Alisar Alkutbi, Nizar A. Al-Shar’i, Waliza Ansar, Prachi Arora, Debasis Bagchi, Manashi Bagchi, Akshay M. Baheti, Vineet Baliga, Vishnu Bhat Ballambattu, Pradipta Banerjee, Priyanka Banerjee, Samudra Prosad Banik, Tejaswini Baral, Sanaa K. Bardaweel, Nicolas Barros, Pijush Basak, Bradford A. Becken, III, M. Bhagyalakshmi, Joyeeta Bhattacharya, Mohini Bhattacharya, Jhimli Bhattacharyya, Maitree Bhattacharyya, Ashmita Bhattacherjee, Karanam Sai Bhavya, Rinchen Doma Bhutia, Geetha Birudala, Ramadevi Birudala, Ayan Biswas, Nabendu Biswas, Sanchita Biswas, Shaoli Biswas, Pobitra Borah, Sayantan Bose, Fernando J. Bula Rudas, Subhendu Chakrabarty, Modhurima Chakraborti, Atreyee Chakraborty, Sanjoy Chakraborty, Shrabastee Chakraborty, Sudipta Chakraborty, S.B. Chandrasekar, Archana Chatterjee, Aritra Chatterjee, Gourab Chatterjee, Rituparna Chatterjee, Tanima Chatterjee, Rameshwar Nath Chaurasia, Bo-Kai Chen, Ashna Chettri, Hui-Fang Chiu, Antara Choudhury, Sailee Chowdhury, Sougata Roy Chowdhury, Courtney Collins, Elaine Colomb, M. Emilio Cuevas-Galindo, Amitava Das, Amlan Das, Arpita Das, Dibya Das, Mousumi Das, Pran Kishore Deb, Sujoy Deb, Anirban Debnath, Satyendra Deka, Shirley F. Delair, Alyssa Delia, Karishma Desai, S. Devaraja, Priyankar Dey, Karma Gurmey Dolma, Bernard William Downs, Jaclyn M. Downs, Lourdes Eguiguren, Mohamed S. El Masry, Elizabeth Estevez-Fregoso, Eunice D. Farfán-García, Zannatul Ferdous, Ramakrishnan Ganesan, Itzel H. García-Coronel, Jazmín García-Machorro, Roseline George, Nandini Ghosh, Rituparna Ghosh, Santanu Ghosh, Arunava Goswami, Karthik Gourishetti, Tanner Guith, Krishna Rao Gurugubelli, Dania Hassan, Sangeeta Hazarika, Vijay Hegde, Ashfaque Hossain, Sheikh Shah Hossain, Amanda L. Hurst, Anahita Jalilvand, Sasmita Jana, Junaid Jibran Jawed, Miguel Jorge, Sedat Kacar, Vikash Kansal, Nabanita Kar, Muhammad Manjurul Karim, Bidita Khandelwal, Ahmet Kilic, Prakash Koirala, Chandrashekhar Kubal, Abhai Kumar, Umesh Kumar, V. Kumar, Leena Kumari, Steve Kushner, Santiago M.C. Lopez, Maxima Madhu, Puja Maitra, Himangshu Sekhar Maji, Sushomasri Maji, Rajib Majumder, Labonya Mandal, Supriya Mandal, Bradford S. McGwire, Odete R. Mendes, Nagendra Babu Mennuru, Sonal Sekhar Miraj, Sutanuka Mitra, Jalal Moludi, Sandipan Mukherjee, Murali Munisamy, Krishna Murti, Monali NandyMazumdar, Masoud Nateqi, Kari A. Neemann, Andrew Nguyen, Aben Ovung, Kunal Pal, Anil T. Pawar, Prakash Narayanan Vasudevan Potty, Megha Rana, Mahadev Rao, Sayantan Ray, Jayati Ray Dutta, Zachary P. Rokop, Sashwati Roy, Brenda A. Rubio-Velazquez, Abinit Saha, Rudra P. Saha, Tiyas Saha, Saptadip Samanta, Saptarshi Sanyal, Dipayan Sarkar, Dipika Sarkar, Riya Sarkar, Alice I. Sato, Abhay R. Satoskar, Abhishek Kumar Sen, Chandan K. Sen, Pracheta Sengupta, Aditi Shah, Dikshya Sharma, Pottathil Shinu, H.N. Shivaprasad, B. Shrikar Reddy, Moumita Sil, Abhilasha Singh, Kanhaiya Singh, Manoj Kumar Singh, Smita Singh, Varun Kumar Singh, N.V.L. Sirisha Mulukuri, Jessica Smith, Marvin A. Soriano-Ursúa, Shruthi Srinivas, Shahnaz Sultana, Arindam Talukdar, Pranathi Tata, Levin Thomas, Jose G. Trujillo-Ferrara, Md. Hafiz Uddin, Muralidhar Varma, Meera Varman, Katharigatta N. Venugopala, Priyanka Verma, Shashidhar Vishwanath, Navya Vyas, Chin-Kun Wang, Jon Wisler, and Nilesh Yadav more...

Published
2023
Full Text
View/download PDF

5. Wnt/β-catenin signaling and p68 conjointly regulate CHIP in colorectal carcinoma

Author

Satadeepa Kal, Shrabastee Chakraborty, Subhajit Karmakar, and Mrinal K. Ghosh

Subjects
Transcriptional Activation, Ubiquitin-Protein Ligases, Cell Cycle, Apoptosis, Cell Biology, Wnt1 Protein, DEAD-box RNA Helicases, Gene Expression Regulation, Neoplastic, Biomarkers, Tumor, Tumor Cells, Cultured, Humans, Colorectal Neoplasms, Promoter Regions, Genetic, Molecular Biology, beta Catenin, Cell Proliferation
Abstract

Emerging evidences suggest abundant expression of Carboxy terminus of Hsc70 Interacting Protein or CHIP (alias STIP1 Homology and U-box Containing Protein 1 or STUB1) in colorectal carcinoma, but the mechanistic detail of this augmented expression pattern is unclear. The signature driver of canonical Wnt pathway, β-catenin, and its co-activator RNA helicase p68, are also overexpressed in colorectal carcinoma. In this study, we describe a novel mechanism of Wnt/β-catenin and p68 mediated transcriptional activation of CHIP gene leading to enhanced proliferation of colorectal carcinoma cells. Bioinformatic analyses reconfirmed an elevated CHIP expression level in colorectal carcinoma datasets. Wnt3A treatment and pharmacological activation of canonical Wnt signaling pathway resulted in increased nuclear translocation of β-catenin, augmenting CHIP expression. Likewise, immunoblotting and Real time PCR following overexpression and knockdown of β-catenin and p68 demonstrated upregulated and downregulated CHIP expression, respectively, at both mRNA and protein levels. p68 along with β-catenin were found to occupy Transcription Factor 4 (TCF4) binding sites on endogenous CHIP promoter and regulate its transcription. After cloning CHIP promoter, the increased and decreased promoter activities of CHIP induced by overexpression and knockdown of either β-catenin or p68 further confirmed transcriptional regulation of CHIP gene by Wnt/β-catenin signaling cascade. Finally, enhanced cellular propagation and migration of colorectal carcinoma cells induced by 'Wnt/β-catenin-p68-CHIP' axis established the significance of this pathway in oncogenesis. To the best of our knowledge, this is the first report elucidating the mechanistic details of transcriptional regulation of CHIP (STUB1) gene expression. more...

Published
2021