Integrin linked kinase (ILK) is a vital signaling protein ubiquitously expressed throughout the body. It binds to intracellular integrins to help promote signaling related to cell adhesion, apoptosis, proliferation, migration, and a plethora of other common cellular functions. In this review, ILKs role in the liver is detailed. Studies have shown ILK to be a major participant in hepatic ECM organization, liver regeneration, insulin resistance, and hepatocellular carcinoma.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8201652PMC
http://dx.doi.org/10.3727/105221621X16113475275710DOI Listing

Publication Analysis

Top Keywords

integrin linked
8
linked kinase
8
kinase ilk
8
role liver
8
ilk role
4
liver pathobiology
4
pathobiology integrin
4
ilk vital
4
vital signaling
4
signaling protein
4

Similar Publications

The tumor microenvironment functions as a dynamic and intricate ecosystem, comprising a diverse array of cellular and non-cellular components that precisely orchestrate pivotal tumor behaviors, including invasion, metastasis, and drug resistance. While unraveling the intricate interplay between the tumor microenvironment and tumor behaviors represents a tremendous challenge, recent research illuminates a crucial biological phenomenon known as cellular mechanotransduction. Within the microenvironment, mechanical cues like tensile stress, shear stress, and stiffness play a pivotal role by activating mechanosensitive effectors such as PIEZO proteins, integrins, and Yes-associated protein.

View Article and Find Full Text PDF

SRF and CBP jointly regulate integrin β6 overexpression in head and neck squamous cell carcinomas.

Cell Signal

January 2025

Department of Basic Medical Science & Department of Stomatology, School of Medicine, Xiamen University, Xiamen, Fujian, China. Electronic address:

Overexpression of integrin β6 (ITGB6) is crucially linked to the invasion and metastasis of head and neck squamous cell carcinoma (HNSCC). The molecular mechanisms driving ITGB6 upregulation in HNSCC are not well understood. Our study comprehensively analyzed the transcriptional regulation and epigenetic modification mechanisms affecting ITGB6 transcription.

View Article and Find Full Text PDF

Tissue-resident memory (T) T cells have emerged as key players in cancer immunosurveillance, and their presence has been linked to a favorable clinical outcome in solid cancer patients. Liver metastases exhibit a highly immunosuppressive tumor microenvironment, however, the role and clinical impact of T cell infiltration in colorectal cancer remain elusive. The expression of several tissue residency and activation biomarkers has been investigated on tumor-infiltrating lymphocytes isolated from 26 patients' colorectal cancer liver metastases (CRC liver metastases) and compared to 16 peripheral blood samples of patients with CRC liver metastases.

View Article and Find Full Text PDF

Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense extracellular matrix (ECM) exhibiting high stiffness and fast stress relaxation. In this work, gelatin-based viscoelastic hydrogels were developed to mimic the compositions, stiffness, and fast stress relaxation of PDAC tissues. The hydrogels were cross-linked by gelatin-norbornene-boronic acid (GelNB-BA), thiolated macromers, and a 1,2-diol-containing linear synthetic polymer PHD.

View Article and Find Full Text PDF

Background: Bioengineering of human teeth for replacement is an appealing regenerative approach in the era of gene therapy. Developmentally regulated transcription factors hold promise in the quest because these transcriptional regulators constitute the gene regulatory networks driving cell fate determination. Atonal homolog 1 (Atoh1) is a transcription factor of the basic helix-loop-helix (bHLH) family essential for neurogenesis in the cerebellum, auditory hair cell differentiation, and intestinal stem cell specification.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!