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Cellular Intrinsic Modulators in the Pathogenesis of Cancer and Inflammatory Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 982

Special Issue Editor


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Guest Editor
Department of Pathology, School of Medicine, Yale University, New Haven, CT 06519, USA
Interests: chronic diseases; immunobiology; infection immunity; signaling; immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cellular signaling pathways within the human body are complex, as cells undergo several physiological changes, and a harmonic co-ordination among the cellular intrinsic modulators is desirable for better functional outcomes. Cellular intrinsic modulators refer to molecules or mechanisms within a cell that regulate its own activities or functions. These modulators can influence various cellular processes, including gene expression, signal transduction, metabolism, and cell growth. Some of the key intrinsic modulators, including kinases, G-proteins, cyclins, ubiquitin ligases, and cell death regulatory proteins, are under constant surveillance of regulatory mechanisms to maintain cellular homeostasis. Perturbations associated with the expression and functionality of intrinsic modulators trigger human diseases, including cancer and inflammatory diseases. Over the past decade, several studies have been carried out to decrypt structural orientation and molecular interactions of intrinsic modulators that can lead to advances in the understanding of cellular complexity. Moreover, methodological and technological modalities now facilitate the simultaneous analysis of genomic and proteomic profiles from the same single cell to better understand cellular mechanisms.

This Special Issue will cover a wide area of research, investigating the molecular and functional characterization of cellular intrinsic modulators in the regulation of cellular pathways and associated pathological manifestations. Authors are welcome to submit original research articles and reviews covering basic, translational, and preclinical studies.

Prof. Chandramani Pathak is a senior scientist, who will assist Dr. Kishu Ranjan in managing this Special Issue. 

Potential topics include (but are not limited to):

  • Transcription factors.
  • Kinases and phosphatases.
  • G-proteins.
  • Second messengers: cyclic AMP (cAMP), calcium ions (Ca2+), and inositol trisphosphate (IP3).
  • MicroRNAs (miRNAs).
  • Epigenetic modifiers: DNA methylation, histone modifications, and chromatin remodeling complexes.
  • Proteases and ubiquitin ligases.
  • Multi-omics (single cell biology).

Dr. Kishu Ranjan
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • cancer
  • immunobiology
  • chronic diseases
  • CRISPR
  • drug discovery
  • multi-omics

Published Papers (1 paper)

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Review

23 pages, 3429 KiB  
Review
Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation
by Kishu Ranjan and Chandramani Pathak
Int. J. Mol. Sci. 2024, 25(6), 3228; https://doi.org/10.3390/ijms25063228 - 12 Mar 2024
Viewed by 796
Abstract
Fas-associated death domain (FADD) is an adaptor protein that predominantly transduces the apoptosis signal from the death receptor (DR) to activate caspases, leading to the initiation of apoptotic signaling and the coordinated removal of damaged, infected, or unwanted cells. In addition to its [...] Read more.
Fas-associated death domain (FADD) is an adaptor protein that predominantly transduces the apoptosis signal from the death receptor (DR) to activate caspases, leading to the initiation of apoptotic signaling and the coordinated removal of damaged, infected, or unwanted cells. In addition to its apoptotic functions, FADD is involved in signaling pathways related to autophagy, cell proliferation, necroptosis, and cellular senescence, indicating its versatile role in cell survival and proliferation. The subcellular localization and intracellular expression of FADD play a crucial role in determining its functional outcomes, thereby highlighting the importance of spatiotemporal mechanisms and regulation. Furthermore, FADD has emerged as a key regulator of inflammatory signaling, contributing to immune responses and cellular homeostasis. This review provides a comprehensive summary and analysis of the cellular dynamics of FADD in regulating programmed cell death and inflammation through distinct molecular mechanisms associated with various signaling pathways. Full article
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