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The Inducible Defense System: The Induction and Development of the Inducible Defence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Michael A. Hickey, Diane Wallace Taylor
As you will recall from chapter 4, macrophages are able to internalize foreign antigen by phagocytosis or pinocytosis. Many cells of the macrophage lineage function as APC. These include monocytes in the blood, histocytes in the connective tissue, macrophages in the spleen, alveolar macrophages in the lungs, and microglial cells in the central nervous system.
Gene Therapy for Lung Cancer
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
Choon Taek Lee, David P. Carbone
A variety of genetic approaches have been used to induce immunity via gene therapy. Allogenic and syngenic major histocompatibility complex (MHC) class I and II genes, costimulatory molecule genes (e.g., B7), and cytokine genes have been inserted to alter the immunological environment and overcome immune defects of cancer patients. These approaches may be viewed as attempts to alter tumor cells so as to make them effective antigen-presenting cells (APC). This is probably oversimplified, but it is a useful model for this discussion.
Colon cancer: pathology and natural history
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
The APC gene has an open reading frame of 8538 base pairs (bp)14 and comprises 15 coding exons, with exon 15 alone containing 6571 bp, making it the largest known human exon. The gene encodes a 2843–residue protein with a molecular weight of 310 kDa14 and wide tissue expression, including stomach, liver, esophagus, kidney, brain and eye. In Figure 4 the principal regions of the APC protein with their functions are schematically reported. This protein, which has a cytoplasmic localization, can be subdivided into two major regions: the carboxy terminal (75%) and the amino terminal (25%), the latter of which contains proline-free blocks with heptad repeats of hydrophobic residues. This pattern is characteristic of α-helical coils and implies protein-protein interactions. In fact, the amino terminus is critical for homo-oligomerization (Figure 4). Most APC gene mutations result in the production of a protein that is truncated at some point beyond residue 171. Thus, the potential for continued oligomerization should generally be preserved in truncated proteins, permitting the formation of inactivating complexes, explaining the dominant negative effect of the mutant protein.
Bioinformatic analysis of the clinicopathological and prognostic significance of oocyte-arresting BTG4 mRNA expression in gynecological cancers
Published in Journal of Obstetrics and Gynaecology, 2023
Hua-chuan Zheng, Hang Xue, Cong-yu Zhang, Rui Zhang
Räty et al. (2011) identified BTG4 as a potential candidate for oocyte developmental competence, as a secreted acidic protein rich in cysteine for cumulus cell expansion. Moreover, Liu et al. (2021) reported that a novel homozygous missense variant in BTG4 causes zygotic cleavage failure and female infertility. Meanwhile, Chu et al. (2012) found that BTG4 had a higher mRNA level in oocytes treated with FSH than in those produced through the natural cycle. Furthermore, Pasternak et al. (2016) demonstrated that the BTG4-CAF1 complex safeguarded metaphase II arrest in mammalian eggs by deadenylating maternal mRNAs. BTG4-depleted eggs progressed into anaphase II spontaneously before fertilization. BTG4 prevented the progression into anaphase by ensuring that the anaphase-promoting complex/cyclosome (APC/C) was completely inhibited during the arrest. These findings indicate that BTG4 may block the cycle progression of oocytes or eggs.
Molecular and cellular pathways in colorectal cancer: apoptosis, autophagy and inflammation as key players
Published in Scandinavian Journal of Gastroenterology, 2022
Lei Yu, Miao-Miao Zhang, Ji-Guang Hou
Mutations in the APC gene appeared as an early primary responsible factor for both hereditary and sporadic forms of CRC. An APC mutation disturbed the proliferation and apoptosis-based homeostasis in colon cells and hampered the ratio between developing cells at the lower region and apoptotic cells at the upper end of the crypts [31,32]. A mutated APC gene disrupted the overall cell multiplication, apoptosis, migration and differentiation. This may have involved a dysregulation of the Wnt pathway and β-catenin-mediated transcription of c-myc (regulates tumorigenesis), cyclin-D1 that bears a key association with overall survival and matrilysin that influences the in vivo invasive and metastatic potential. Additionally, participation of peroxisome proliferator-activated receptor that appears pertinent to the pathophysiology of inflammatory diseases and multidrug resistance, MDR1, that showed a significantly decreased activity in primary colorectal cancer samples in comparison to the normal mucosa was important [33].
Bone morphogenetic protein (BMP) 7 expression is regulated by the E3 ligase UBE4A in diabetic nephropathy
Published in Archives of Physiology and Biochemistry, 2020
Ying Feng, Ming-Yue Jin, Dong-Wei Liu, Li Wei
UBE4A and UBE4B are U-box-containing ubiquitylation enzymes and are the two human homologues of yeast UFD2 ubiquitination factor. They have been shown to be mutated in different cancer, including neuroblastoma and colorectal cancer (Caren et al.2006; Naudin et al.2014). The yeast homologue Ufd2 has been shown to ubiquitylate and degrade the cell cycle kinase Mps1 that is a core component of the anaphase promoting complex E3, and that this function is conserved in humans (Liu et al.2011). UBE4A expression has also been shown to be dependent on cell cycle progression (Contino et al.2004), substantiating its role on cell growth and proliferation. However, role of UBE4A has not been previously elucidated in the context of DN.