Jasreen Uppal

Dr. Jasreen Uppal

orcid

Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 November 2022 in Journal of Heterocyclic Chemistry
Verified
Journal Article
Closed access
JUJasreen Uppal
Jasreen Uppal
PMPrince Ahad Mir
Prince Ahad Mir
ACApporva Chawla
Apporva Chawla
NKNishant Kumar
Nishant Kumar
GKGurinder Kaur
Gurinder Kaur
DBDivya Dhawal Bhandari
Divya Dhawal Bhandari

27 August 2025 in Pharmaceuticals
Verified
Journal Article
Open access
PDF file
AWAdil Farooq Wali
Adil Farooq Wali
AAAbid Reza Ansari
Abid Reza Ansari
PMPrince Ahad Mir
Prince Ahad Mir
Mohamed El-TananiMohamed El-Tanani
Mohamed El-Tanani
RBRasha Babiker
Rasha Babiker
REYAZ HASSAN MIRREYAZ HASSAN MIR
REYAZ HASSAN MIR
Hepatocellular carcinoma (HCC), the most prevalent primary liver cancer, continues to pose a significant global health burden due to its high mortality rate. In addition to genetic alterations, epigenetic aberrations, including DNA methylation, histone modifications, chromatin remodeling, and noncoding RNA (ncRNA) dysregulation, play critical roles in HCC initiation and progression. Notably, miR-375 and miR-483-5p are among the most dysregulated miRNAs in HCC, with their altered expression levels closely associated with tumor stage and patient survival. These epigenetic modifications offer promising therapeutic avenues due to their reversibility and dynamic nature. Furthermore, specific epigenetic signatures such as CDH1 promoter hypermethylation and HOTAIR overexpression are being explored as potential biomarkers for early detection and treatment response. In this chapter, we review recent advances in the epigenetic landscape of HCC and discuss their diagnostic and therapeutic implications, highlighting their potential to improve patient outcomes through personalized medicine approaches.

31 March 2023 in Metabolites
Verified
Journal Article
Open access
PDF file
REYAZ HASSAN MIRREYAZ HASSAN MIR
REYAZ HASSAN MIR
PMPrince Ahad Mir
Prince Ahad Mir
JUJasreen Uppal
Jasreen Uppal
ACApporva Chawla
Apporva Chawla
Patel MiteshPatel Mitesh
Patel Mitesh
RMRoohi Mohi-ud-din
Roohi Mohi-ud-din
Homeostasis between protein synthesis and degradation is a critical biological function involving a lot of precise and intricate regulatory systems. The ubiquitin-proteasome pathway (UPP) is a large, multi-protease complex that degrades most intracellular proteins and accounts for about 80% of cellular protein degradation. The proteasome, a massive multi-catalytic proteinase complex that plays a substantial role in protein processing, has been shown to have a wide range of catalytic activity and is at the center of this eukaryotic protein breakdown mechanism. As cancer cells overexpress proteins that induce cell proliferation, while blocking cell death pathways, UPP inhibition has been used as an anticancer therapy to change the balance between protein production and degradation towards cell death. Natural products have a long history of being used to prevent and treat various illnesses. Modern research has shown that the pharmacological actions of several natural products are involved in the engagement of UPP. Over the past few years, numerous natural compounds have been found that target the UPP pathway. These molecules could lead to the clinical development of novel and potent anticancer medications to combat the onslaught of adverse effects and resistance mechanisms caused by already approved proteasome inhibitors. In this review, we report the importance of UPP in anticancer therapy and the regulatory effects of diverse natural metabolites, their semi-synthetic analogs, and SAR studies on proteasome components, which may aid in discovering a new proteasome regulator for drug development and clinical applications.

12 July 2022 in Chemical Biology & Drug Design
Verified
Journal Article
Closed access
GKGurinder Kaur
Gurinder Kaur
ASAtamjit Singh
Atamjit Singh
GAGeetakshi Arora
Geetakshi Arora
AMAditi Monga
Aditi Monga
AJAnupmjot Kaur Jassal
Anupmjot Kaur Jassal
KBKundan Singh Bora
Kundan Singh Bora

Verified
Journal Article
Open access
PDF file
Abdul Jalil ShahAbdul Jalil Shah
Abdul Jalil Shah
MDMOHAMMAD YOUNIS DAR
MOHAMMAD YOUNIS DAR
BJBisma Hussain Jan
Bisma Hussain Jan
IQInsha Qadir
Insha Qadir
REYAZ HASSAN MIRREYAZ HASSAN MIR
REYAZ HASSAN MIR
MMMUBASHIR MASOODI
MUBASHIR MASOODI
Alzheimer’s disease (AD) is a brain disorder that is more prevalent in developed nations and remains one of most intractable conditions so far. It is characterized by a gradual onset, a prolonged progression, and an unclear pathophysiology. At the present time, there are no effective treatments available for the disease. However, human neural stem cells (hNSCs) have the capacity to substitute lost neurons in a functional manner, strengthen synaptic networks that have been compromised, and repair the damaged brain. Due to the unavailability of restorative therapeutics, there is a significant global burden on the economy. When it comes to the treatment of neurodegenerative diseases, NSCs provide a potentially game-changing approach to treating Alzheimer’s disease. Through the delivery of trophic factors that promote the viability and regeneration of lost neurons in experimental animals suffering from neurodegenerative disorders, these treatments have the potential to facilitate beneficial recuperation. Positive restorative outcomes may be achieved in a variety of ways, including the replacement of lost cells, the combining of cells, the secretion of neurotrophic factors, the formation of endogenous stem cells, and transdifferentiation. Conversely, there are obstacles that need to be overcome before NSC-based treatments can be used in clinical settings. This review article discusses current developments in the use of neural stem cells (NSCs) for the treatment of Alzheimer’s disease (AD). In addition, we highlight the difficulties and opportunities that are involved with the use of neural stem cell transplant treatment for Alzheimer’s disease.