SLC35B2

Last update 08 May 2025

Basic Info

Synonyms

Adenosine 3'-phospho 5'-phosphosulfate transporter 1, PAPS transporter 1, PAPST1

+ [7]

Introduction

Probably functions as a 3'-phosphoadenylyl sulfate:adenosine 3',5'-bisphosphate antiporter at the Golgi membranes. Mediates the transport from the cytosol into the lumen of the Golgi of 3'-phosphoadenylyl sulfate/adenosine 3'-phospho 5'-phosphosulfate (PAPS), a universal sulfuryl donor for sulfation events that take place in that compartment.

100 Clinical Results associated with SLC35B2

100 Translational Medicine associated with SLC35B2

0 Patents (Medical) associated with SLC35B2

Literatures (Medical) associated with SLC35B2

01 Feb 2025·Hepatology

Enhanced SLC35B2/SAV1 sulfation axis promotes tumor growth by inhibiting Hippo signaling in HCC

Article

Author: Li, Bowen ; Huang, Zhao ; Wang, Kui ; Duan, Xirui ; Wang, Longqin ; He, Bo ; Jiang, Jingwen ; Liu, Rui ; Ye, Qin ; Huang, Canhua ; Qin, Siyuan ; Peng, Peilan

Background and Aims:Protein tyrosine sulfation (PTS) is a common posttranslational modification that regulates a variety of physiological and pathological processes. However, the role of PTS in cancer remains poorly understood. The goal of this study was to determine whether and how PTS plays a role in HCC progression.Approach and Results:By mass spectrometry and bioinformatics analysis, we identified SAV1 as a novel substrate of PTS in HCC. Oxidative stress upregulates the transcription of SLC35B2, a Golgi-resident transporter of sulfate donor 3ʹ-phosphoadenosine 5ʹ-phosphosulfate, leading to increased sulfation of SAV1. Sulfation of SAV1 disrupts the formation of the SAV1-MST1 complex, resulting in a decrease of MST1 phosphorylation and subsequent inactivation of Hippo signaling. These molecular events ultimately foster the growth of HCC cells both in vivo and in vitro. Moreover, SLC35B2 is a novel transcription target gene of the Hippo pathway, constituting a positive feedback loop that facilitates HCC progression under oxidative stress.Conclusions:Our findings reveal a regulatory mechanism of the SLC35B2/SAV1 sulfation axis in response to oxidative stress, highlighting its potential as a promising therapeutic target for HCC.

17 Jul 2024·Science Translational Medicine

Molecular dissection of cobra venom highlights heparinoids as an antidote for spitting cobra envenoming

Article

Author: Albulescu, Laura-Oana ; Bartlett, Keirah E. ; Patel, Karishma ; Kurdyukov, Sergey ; Du, Tian Y. ; Dawson, Charlotte A. ; Rasmussen, Sean A. ; Gutiérrez, José María ; Marriott, Amy E. ; Crittenden, Edouard ; Westhorpe, Adam P. ; Wilkinson, Mark C. ; Moreno, Cesar L. ; Casewell, Nicholas R. ; Denes, Christopher E. ; Neely, G. Gregory ; Chung, Felicity ; Hall, Steven R. ; Mackay, Joel P.

Snakebites affect about 1.8 million people annually. The current standard of care involves antibody-based antivenoms, which can be difficult to access and are generally not effective against local tissue injury, the primary cause of morbidity. Here, we used a pooled whole-genome CRISPR knockout screen to define human genes that, when targeted, modify cell responses to spitting cobra venoms. A large portion of modifying genes that conferred resistance to venom cytotoxicity was found to control proteoglycan biosynthesis, including EXT1 , B4GALT7 , EXT2 , EXTL3 , XYLT2 , NDST1 , and SLC35B2 , which we validated independently. This finding suggested heparinoids as possible inhibitors. Heparinoids prevented venom cytotoxicity through binding to three-finger cytotoxins, and the US Food and Drug Administration–approved heparinoid tinzaparin was found to reduce tissue damage in mice when given via a medically relevant route and dose. Overall, our systematic molecular dissection of cobra venom cytotoxicity provides insight into how we can better treat cobra snakebite envenoming.

01 Jun 2024·Tissue and Cell

Characterization of a spontaneous osteopetrosis model using RANKL-dysfunctional mice

Article

Author: Kim, Beom Chang ; Ju, Jiwoong ; Lim, Wonbong ; Lee, Gwangchul ; Jang, Yuria ; Lee, Chang-Moon ; Kim, Dae Ok

Tumor necrosis factor superfamily member 11 (TNFSF11), or receptor activator of nuclear factor-κB ligand (RANKL), is a crucial osteoclast-stimulating factor binding to RANK on osteoclast membranes. Mouse models are powerful tools for understanding the genetic mechanisms of related diseases. Here, we examined the utility of Tnfsf11 mutation in mice for understanding the mechanisms of bone remodeling and dysmorphology. The Tnfsf11gum mouse, discovered in 2011 at Jackson Laboratory, was used to study the genetic landscape associated with TNFSF11 inactivation in bone marrow tissues. Tnfsf11^gum/+ and Tnfsf11^+/+ mice were subjected to Micro-CT observation, ELISA analysis, histological evaluation, and massively-parallel mRNA sequencing (RNA-Seq) analysis. Tnfsf11^gum/+ mice exhibited severe osteopetrotic changes in the bone marrow cavity, along with significantly lower serum RANKL levels and a reduced number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in the bone marrow compared to those in Tnfsf11^+/+ mice. However, tooth eruption between Tnfsf11^gum/+ and Tnfsf11^+/+ mice did not differ. Furthermore, genes involved in osteoblast proliferation and differentiation, including Gli1, Slc35b2, Lrrc17, and Junb were differentially expressed. Heterozygous mutation of TNFSF11 was also associated with a slightly increased expression of genes involved in osteoclast proliferation and differentiation, including Tcirg1, Junb, Anxa2, and Atp6ap1. Overall, we demonstrate that single gene mutations in Tnfsf11 cause bone resorption instability without significantly altering the genes related to osteoblast and osteoclast activity in the bone marrow cavity, thus establishing an optimal resource as an experimental animal model for bone resorption in bone biology research.

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SLC35B2

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