Ask about this productRelated genes to: TM4SF20 antibody
- Gene:
- TM4SF20 NIH gene
- Name:
- transmembrane 4 L six family member 20
- Previous symbol:
- -
- Synonyms:
- FLJ22800, TCCE518
- Chromosome:
- 2q36.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-21
- Date modifiied:
- 2014-11-19
Related products to: TM4SF20 antibody
Related articles to: TM4SF20 antibody
- Lymph node metastasis is one of the important factors affecting the prognosis of lung adenocarcinoma (LUAD) patients. The key molecules in lymph node metastasis have not yet been fully revealed. Therefore, we aimed to construct a prognostic model based on lymph node metastasis-related genes to evaluate the prognosis of LUAD patients. - Source: PubMed
Publication date: 2023/04/10
Li QiaoLiu Xiao-LiJiang NiLi Qian-YunSong Yong-XiangKe Xi-XianHan HaoLuo QianGuo QiangLuo Xiang-YuChen Cheng - Transmembrane proteins must adopt proper topology to perform their functions. We previously demonstrated that ceramide regulates TM4SF20 (transmembrane 4 L6 family 20) by altering the topology of the transmembrane protein, but the underlying mechanism remains obscure. Here we report that TM4SF20 is synthesized in the endoplasmic reticulum (ER) with a cytosolic C terminus and a luminal loop before the last transmembrane helix where N132, N148, and N163 are glycosylated. In the absence of ceramide, the sequence surrounding glycosylated N163 but not N132 is retrotranslocated from lumen to cytosol independent of ER-associated degradation. Accompanying this retrotranslocation, the C terminus of the protein is relocated from cytosol to lumen. Ceramide delays the retrotranslocation process, causing accumulation of the protein that is originally synthesized. Our findings suggest that N-linked glycans, although synthesized in the lumens, may be exposed to cytosol through retrotranslocation, a reaction that may play a crucial role in topological regulation of transmembrane proteins. - Source: PubMed
Publication date: 2023/03/26
Wang JingchengHan SungwonYe Jin - Congenital hepatic fibrosis / Autosomal recessive polycystic kidney disease (CHF/ARPKD) is an inherited neonatal disease induced by mutations in the gene and characterized by cysts, and robust pericystic fibrosis in liver and kidney. The PCK rat is an excellent animal model which carries a mutation and exhibits similar pathophysiology. We performed RNA-Seq analysis on liver samples from PCK rats over a time course of postnatal day (PND) 15, 20, 30, and 90 using age-matched Sprague-Dawley (SD) rats as controls to characterize molecular mechanisms of CHF/ARPKD pathogenesis. A comprehensive differential gene expression (DEG) analysis identified 1298 DEGs between PCK and SD rats. The genes overexpressed in the PCK rats at PND 30 and 90 were involved cell migration (e.g. , and ), cell adhesion (e.g. , and ), and wound healing (e.g. ). Connective tissue growth factor ( ) and platelet-derived growth factor ( ), two genes associated with fibrosis, were upregulated in PCK rats at all time-points. Genes associated with MHC class I molecules (e.g. ) or involved in ribosome assembly (e.g. ) were significantly downregulated in PCK rats. Upstream regulator analysis showed activation of proteins involved tissue growth (MTPN) and inflammation (STAT family members) and chromatin remodeling (BRG1), and inhibition of proteins involved in hepatic differentiation (HNF4α) and reduction of fibrosis (SMAD7). The increase in mRNAs of four top upregulated genes including , and was confirmed at the protein level using immunohistochemistry. In conclusion, these studies indicate that a combination of increased inflammation, cell migration and wound healing, and inhibition of hepatic function, decreased antifibrotic gene expression are the major underlying pathogenic mechanisms in CHF/ARPKD. - Source: PubMed
Publication date: 2023/01/20
Khare SatyajeetJiang LuCabrara Diego PaineApte UdayanPritchard Michele T - Language impairment (LI) is highly heritable and aggregates in families. Genetic investigation of LI has revealed many chromosomal regions and genes of interest, though very few studies have focused on rare variant analysis in non-English speaking or non-European samples. We selected four candidate genes ( and ) strongly suggested for specific language impairment (SLI), a subtype of LI, and investigated rare protein coding variants through Sanger sequencing of probands with LI ascertained from Pakistan. The probands and their family members completed a speech and language family history questionnaire and a vocabulary measure, the Peabody Picture Vocabulary Test-fourth edition (PPVT-4), translated to Urdu, the national language of Pakistan. Our study aimed to determine the significance of rare variants in these SLI candidate genes through segregation analysis in a novel population with a high rate of consanguinity. In total, we identified 16 rare variants (according to the rare MAF in the global population in gnomAD v2.1.1 database exomes), including eight variants with a MAF <0.5 % in the South Asian population. Most of the identified rare variants aggregated in proband's families, one rare variant (c.*9T>C in ) co-segregated in a small family (PKSLI-64) and another (c.2465C>T in ) co-segregated in the proband branch (PKSLI-27). The lack of complete co-segregation of most of the identified rare variants indicates that while these genes could be involved in overall risk for LI, other genes are likely involved in LI in this population. Future investigation of these consanguineous families has the potential to expand our understanding of gene function related to language acquisition and impairment. - Source: PubMed
Publication date: 2021/08/27
Andres Erin MNeely Heather LHafeez HumaYasmin TahiraKausar FarzanaBasra M Asim RazaRaza Muhammad Hashim - Transmembrane proteins must adopt a proper topology to execute their functions. In mammalian cells, a transmembrane protein is believed to adopt a fixed topology. This assumption has been challenged by recent reports that ceramide or related sphingolipids regulate some transmembrane proteins by inverting their topology. Ceramide inverts the topology of certain newly synthesized polytopic transmembrane proteins by altering the direction through which their first transmembrane helices are translocated across membranes. Thus, this regulatory mechanism has been designated as Regulated Alternative Translocation (RAT). The physiological importance of this topological regulation has been demonstrated by the finding that ceramide-induced RAT of TM4SF20 (Transmembrane 4 L6 family member 20) is crucial for the effectiveness of doxorubicin-based chemotherapy, and that dihydroceramide-induced RAT of CCR5 (C-C chemokine receptor type 5), a G protein-coupled receptor, is required for lipopolysaccharide (LPS) to inhibit chemotaxis of macrophages. These observations suggest that topological inversion through RAT could be an emerging mechanism to regulate transmembrane proteins. - Source: PubMed
Ye Jin