OLAH

Last update 08 May 2025

Basic Info

Synonyms

Augmented in rheumatoid arthritis 1, AURA1, FLJ11106

+ [9]

Introduction

Contributes to the release of free fatty acids from fatty acid synthase (FASN). Has broad substrate specificity, giving rise to a range of free fatty acids with chain lengths between 10 and 16 carbon atoms (C10 - C16).

100 Clinical Results associated with OLAH

100 Translational Medicine associated with OLAH

0 Patents (Medical) associated with OLAH

Literatures (Medical) associated with OLAH

01 Dec 2025·Journal of Mammary Gland Biology and Neoplasia

Disease-Associated Mutations of the STAT5B SH2 Domain Regulate Cytokine-Driven Enhancer Function and Mammary Development

Article

Author: Liu, Chengyu ; Jankowski, Jakub ; Hennighausen, Lothar ; Lee, Hye Kyung

AbstractMammary gland development during pregnancy is controlled by lactogenic hormones via the JAK2-STAT5 pathway. Gene deletion studies in mice have revealed the crucial roles of both STAT5A and STAT5B in establishing the genetic programs necessary for the development of mammary epithelium and successful lactation. Several hundred single nucleotide polymorphisms (SNPs) have been identified in human STAT5B, although their pathophysiological significance remains largely unknown. The SH2 domain is vital for STAT5B activation, and this study focuses on the impact of two specific missense mutations identified in T cell leukemias, the substitution of tyrosine 665 with either phenylalanine (Y665F) or histidine (Y665H). By introducing these human mutations into the mouse genome, we uncovered distinct and opposite functions. Mice harboring the STAT5BY665H mutation failed to develop functional mammary tissue, resulting in lactation failure, while STAT5BY665F mice exhibited accelerated mammary development during pregnancy. Transcriptomic and epigenomic analyses identified STAT5BY665H as Loss-Of-Function (LOF) mutation, impairing enhancer establishment and alveolar differentiation, whereas STAT5BY665F acted as a Gain-Of-Function (GOF) mutation, elevating enhancer formation. Persistent hormonal stimulation through two pregnancies led to the establishment of enhancer structures, gene expression and successful lactation in STAT5BY665H mice. Lastly, we demonstrate that Olah, a gene known to drive life-threatening viral disease in humans, is regulated by STAT5B through a candidate four-partite super-enhancer. In conclusion, our findings underscore the role of human STAT5B variants in modulating mammary gland homeostasis and their critical impact on lactation.

01 Mar 2025·Immunology & Cell Biology

Increased fatty acid production and macrophage‐driven inflammation as key drivers of severe respiratory disease

Article

Author: Mueller, Ivo ; Eriksson, Emily M

In this article, we discuss a recent article by Jia et al., where high OLAH expression was detected in severe and fatal respiratory disease which was associated with a number of processes and responses. These include high abundance of oleic acid, excessive cytokine release, high viral titres and lipid droplets and increased presence of lung-associated innate cells.

01 Jan 2025·Zoological Research

Multi-omics analysis and experimental verification reveal testicular fatty acid metabolism disorder in non-obstructive azoospermia

Article

Author: Yao, Bing ; Ge, Xie ; Ma, Jin-Zhao ; Zou, Zhi-Chuan ; Feng, Yu-Ming ; Chen, Wei-Qing ; Jing, Jun ; Wang, Hui ; Li, Zhou ; Xiang, Yi-Jian

Increasing evidence implicates disruptions in testicular fatty acid metabolism as a contributing factor in non-obstructive azoospermia (NOA), a severe form of male infertility. However, the precise mechanisms linking fatty acid metabolism to NOA pathogenesis have not yet been fully elucidated. Multi-omics analyses, including microarray analysis, single-cell RNA sequencing (scRNA-seq), and metabolomics, were utilized to investigate disruptions in fatty acid metabolism associated with NOA using data from public databases. Results identified ACSL6, ACSBG2, and OLAH as key genes linked to fatty acid metabolism dysregulation, suggesting their potential causative roles in NOA. A marked reduction in omega-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), was observed, potentially contributing to the pathological process of NOA. Sertoli cells in NOA patients exhibited apparent fatty acid metabolic dysfunction, with PPARG identified as a key transcription factor (TF) regulating this process. Functional analyses demonstrated that PPARG is crucial for maintaining blood-testis barrier (BTB) integrity and promoting spermatogenesis via regulation of fatty acid metabolism. These findings reveal the pivotal role of fatty acid metabolism in NOA and identify PPARG as a potential therapeutic target.

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OLAH

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