TMEM170A

Last update 08 May 2025

Basic Info

Synonyms

FLJ37611, TMEM170, TMEM170A

+ [1]

Introduction

Acts as a regulator of endoplasmic reticulum (ER) and nuclear envelope (NE) morphogenesis. Affects the ratio between tubular ER and ER sheets by promoting sheet formation at the expense of tubules. Influences NE expansion, nuclear pore complex formation and proper localization of inner nuclear membrane proteins (PubMed:26906412).

100 Clinical Results associated with TMEM170A

100 Translational Medicine associated with TMEM170A

0 Patents (Medical) associated with TMEM170A

Literatures (Medical) associated with TMEM170A

01 Jan 2021·AMIA ... Annual Symposium proceedings. AMIA Symposium

Gene-Based Analysis Reveals Sex-Specific Genetic Risk Factors of COPD.

Article

Author: Joo, Jaehyun ; Himes, Blanca

Sex-specific differences have been noted among people with chronic obstructive pulmonary disease (COPD), but whether these differences are attributable to genetic variation is poorly understood. The availability of large biobanks with deeply phenotyped subjects such as the UK Biobank enables the investigation of sex-specific genetic associations that may provide new insights into COPD risk factors. We performed sex-stratified genome-wide association studies (GWAS) of COPD (male: 12,958 cases and 95,631 controls; female: 11,311 cases and 123,714 controls) and found that while most associations were shared between sexes, several regions had sex-specific contributions, including respiratory viral infection-related loci in/near C5orf56 and PELI1. Using the newly developed R package 'snpsettest', we performed gene-based association tests and identified gene-level sex-specific associations, including C5orf56 on 5q31.1, CFDP1/TMEM170A/CHST6 on 16q23.1 and ASTN2/TRIM32 on 9q33.1. Our results identified promising genes to pursue in functional studies to better understand sexual dimorphism in COPD.

01 Oct 2020·JNCI: Journal of the National Cancer InstituteQ1 · MEDICINE

A Transcriptome-Wide Association Study Identifies Novel Candidate Susceptibility Genes for Pancreatic Cancer

Q1 · MEDICINE

Article

Author: Giles, Graham G ; Neale, Rachel E ; Wolpin, Brian M ; Duell, Eric J ; Chung, Charles C ; Patel, Alpa V ; Albanes, Demetrius ; Severi, Gianluca ; Rothman, Nathaniel ; Sund, Malin ; Sieri, Sabina ; Goggins, Michael ; Childs, Erica J ; Porta, Miquel ; Haiman, Christopher ; Jermusyk, Ashley ; Goodman, Phyllis J ; Thornquist, Mark D ; Silverman, Debra ; Brais, Lauren ; Klein, Alison P ; Jacobs, Eric J ; Yu, Herbert ; Yuan, Chen ; Oberg, Ann L ; Li, Donghui ; Scelo, Ghislaine ; Berndt, Sonja ; Mocci, Evelina ; Chatterjee, Nilanjan ; Tobias, Geoffrey S ; Klein, Eric A ; Bueno-de-Mesquita, Bas ; Helzlsouer, Kathy J ; Risch, Harvey A ; Andreotti, Gabriella ; Yu, Kai ; Wentzensen, Nicolas ; Goodman, Gary E ; Brennan, Paul ; Wactawski-Wende, Jean ; Van Den Eeden, Stephen K ; Zeleniuch-Jacquotte, Anne ; Malats, Núria ; Zhong, Jun ; Hasan, Manal ; Buring, Julie ; Song, Lei ; Männistö, Satu ; Fuchs, Charles ; Hartge, Patricia ; Bamlet, William R ; Collins, Irene ; Milne, Roger ; LeMarchand, Loic ; Arslan, Alan A ; Cotterchio, Michelle ; Gallinger, Steven ; Zheng, Wei ; Ng, Kimmie ; Babic, Ana ; Zhang, Mingfeng ; Du, Mengmeng ; Gaziano, J Michael ; Hoover, Robert ; Kraft, Peter ; Beane-Freeman, Laura ; Brown, Kevin ; Stolzenberg-Solomon, Rachael Z ; Giovannucci, Edward ; Tjønneland, Anne ; Smith, Jill P ; Wu, Lang ; Canzian, Federico ; Peters, Ulrike ; Chanock, Stephen J ; Petersen, Gloria M ; Trichopoulou, Antonia ; Kurtz, Robert J ; Xiao, Wenming ; Holly, Elizabeth A ; Amundadottir, Laufey T ; Shi, Jianxin ; Borgida, Ayelet ; Kogevinas, Manolis ; Kooperberg, Charles ; Visvanathan, Kala ; Zhang, Tongwu ; Orlow, Irene ; White, Emily ; Bracci, Paige M ; Obazee, Ofure ; Hoskins, Jason W ; Shu, Xiao-Ou ; Sesso, Howard D

AbstractBackgroundAlthough 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown.MethodsTo discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74–421 samples).ResultsWe identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate < .05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22: RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction.ConclusionsBy integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.

15 Apr 2016·Journal of Cell Science

Transmembrane protein TMEM170A is a newly discovered regulator of ER and nuclear envelope morphogenesis in human cells

Article

Author: Christodoulou, Andri ; Santama, Niovi ; Mattaj, Iain W. ; Santarella-Mellwig, Rachel

ABSTRACTThe mechanism of endoplasmic reticulum (ER) morphogenesis is incompletely understood. ER tubules are shaped by the reticulons (RTNs) and DP1/Yop1p family members, but the mechanism of ER sheet formation is much less clear. Here, we characterize TMEM170A, a human transmembrane protein, which localizes in ER and nuclear envelope membranes. Silencing or overexpressing TMEM170A in HeLa K cells alters ER shape and morphology. Ultrastructural analysis reveals that downregulation of TMEM170A specifically induces tubular ER formation, whereas overexpression of TMEM170A induces ER sheet formation, indicating that TMEM170A is a newly discovered ER-sheet-promoting protein. Additionally, downregulation of TMEM170A alters nuclear shape and size, decreases the density of nuclear pore complexes (NPCs) in the nuclear envelope and causes either a reduction in inner nuclear membrane (INM) proteins or their relocalization to the ER. TMEM170A interacts with RTN4, a member of the reticulon family; simultaneous co-silencing of TMEM170A and RTN4 rescues ER, NPC and nuclear-envelope-related phenotypes, implying that the two proteins have antagonistic effects on ER membrane organization, and nuclear envelope and NPC formation.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

TMEM170A

Basic Info

Related

Analysis