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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.
Familial Adenomatous Polyposis
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Paul Kolarsick, Steven D. Wexner
Adenomatous polyposis coli encodes a protein in the Wnt pathway, which signals the ubiquination and degradation of the β-catenin oncoprotein. In the absence of the APC protein product, β-catenin accumulates in the nucleus leading to unregulated cell proliferation. In addition, the APC protein product functions in microtubule stabilization during cell division; a defective gene leads to abnormal chromosomal segregation and aberrant mitosis [1].
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.
Mutations of key driver genes in gastric cancer metastasis risk: a systematic review and meta-analysis
Published in Expert Review of Molecular Diagnostics, 2021
Jin Wang, Xinye Shao, Yang Liu, Ruichuan Shi, Bowen Yang, Jiawen Xiao, Yunpeng Liu, Xiujuan Qu, Zhi Li
The APC gene is closely related to the incidence of colorectal cancer (CRC) and mutations have been seen in over 80% of CRC patients. The inactivation of APC is also considered a key early event in the occurrence of sporadic CRC [66]. Partial loss of APC function was found to lead to activation of the classical WNT pathway and the occurrence of intestinal tumors [67]. It has also been demonstrated that APC mutations play a central role in the development of some GC subtypes, such as signet-ring cell carcinomas and differentiated adenocarcinomas [68,69]. However, even in CRC, the relationship between APC mutation and metastasis remains unclear. A recent meta-analysis showed no significant relationship between APC mutations and CRC metastasis [70]. Although APC is classified as a tumor-suppressor gene, simple mutations of tumor suppressor genes do not necessarily promote metastasis. In the present study, an interesting result showed that APC mutations had a significant protective effect on GC lymph nodes and distant metastasis. The findings were consistent with hypermethylation of APC which was related to a lower number of metastasized lymph nodes in esophageal squamous cell carcinoma [71].
The role of microtubules in the regulation of epithelial junctions
Published in Tissue Barriers, 2018
Ekaterina Vasileva, Sandra Citi
APC is a gene mutated in familial colorectal cancer, which encodes a large protein involved in the regulation of the cytoplasmic pool of β-catenin.144 APC binds to MTs, either directly or through the +TIPs EB1 or CLIP170, and its binding to MTs is regulated by phosphorylation, and results in MT polymerization and stabilization145-149 (Figure 3). Studies on cultured cells show that two spatially separate populations of APC exist at the cell periphery, one which is highly dynamic and associates with MTs near free edges, and a second comparatively static and closely associated with actin at sites of cell-cell contact150,151 (Figure 3). However, the molecular basis for APC association with junctions, and how the junctional localization of APC is related to its signaling activity is not clear.