SLC12A2 antibody
- Known as:
- SLC12A2 (anti-)
- Catalog number:
- orb20466
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SLC12A2 antibody
Related genes to: SLC12A2 antibody
- Gene:
- SLC12A2 NIH gene
- Name:
- solute carrier family 12 member 2
- Previous symbol:
- -
- Synonyms:
- NKCC1, BSC, BSC2, PPP1R141
- Chromosome:
- 5q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-02-17
Related products to: SLC12A2 antibody
Related articles to: SLC12A2 antibody
- The Hilsa Shad is an anadromous fish of major ecological and economic importance in Bangladesh. It migrates between marine and freshwater environments and faces substantial osmotic challenges. There is limited research on osmoregulatory gene expression during migration across diverse habitats. This study provides the first genome-wide identification of the Slc12a2 gene in Hilsa Shad and confirms the existence of two Slc12a2 gene paralogs. To evaluate their potential role in salinity adaptation, we further examined their expression across contrasting habitats. The Bay of Bengal where the fish originates, the genome-wide expression of Slc12a2 has not yet been investigated. The Surma River has been identified as a significant freshwater habitat for Hilsa Shad. However, the molecular information including gene expression data has not yet been reported for this population. In this study, RT-qPCR was used to analyze gill, kidney, liver, and muscle tissues of Hilsa Shad. The results showed that both Slc12a2 paralogs were significantly down-regulated during upstream migration from the Bay to Bengal to the Surma River. These findings demonstrate the essential role of Slc12a2 in maintaining osmotic balance during habitat transition. This genome-wide approach also gives an overall picture of how multiple Slc12a2 gene copies respond to environmental salinity changes and regulate homeostasis. - Source: PubMed
Publication date: 2026/06/03
Aunkor Md Toasin HossainAlam Md JahangirZidan Musfiq AhamedKhan Mohammad Mehedi HasanKabir Muhammad AnamulMiah Md Faruque - Cajal-Retzius neurons (CRN) represent an early-born transient neuronal population in the mammalian neocortex. They are best known for secreting reelin, which is essential for neuronal migration and layer formation in the developing cortex. However, their functional integration into developing cortical circuits and their contribution to early network dynamics have been poorly understood. In this study, we investigated the structural and functional integration of CRN into developing neocortical networks with immunohistochemistry, three-dimensional reconstruction of GABAergic inputs, extracellular electrophysiology and calcium imaging. In addition, multiplexed FISH was used to determine the expression levels of the chloride transporters NKCC1 and KCC2 in CRN at different postnatal stages. Finally, we employed optogenetic stimulation to assess the functional and developmental consequences of CRN activation. We found that CRN receive dense dendritic GABAergic synaptic inputs at early postnatal stages. Functional analyses revealed that a substantial fraction of CRN is spontaneously active, and that their activity is synchronized with both CRN and non-CRN neurons. At the molecular level, they display a persistent NKCC1-dominant expression profile. This profile can contribute to the excitatory GABA responses, but also affect their cell death, as chronic blockade of NKCC1 was associated with reduced CRN loss in vitro. Acute optogenetic activation of CRN at early stages increased network excitability in organotypic neocortical cultures and induced stimulus-evoked field responses, while chronic activation at later time points accelerated CRN loss. Overall, these findings demonstrate that, during development, dense GABAergic input connectivity, coupled with the putative excitatory action of GABA, can engage CRN in early network activity. Furthermore, not only do CRN actively participate in early immature circuits, but their activity also amplifies spontaneous network dynamics and contributes to their own transience, highlighting a potential novel functional role of CRN during neocortical development. - Source: PubMed
Publication date: 2026/09/09
De Rosa FedericoKilb WernerLuhmann Heiko JSinning Anne - Solute carrier (SLC) transporters comprise a family of >450 membrane-bound proteins that facilitate the transport of a wide array of substrates across biological membranes. They play a fundamental role in controlling the transport of molecules, such as ions and metabolites, across the cell membranes. Despite the availability of marketed drugs targeting well-known SLC transporters, such as neurotransmitter (i.e. SERT, NET, DAT) and glucose (GLUTs) transporters, most of the SLCs are still under-investigated as therapeutic targets. A major limiting factor in this area is the lack of suitable assays and tools that enable High Throughput Screening (HTS) of large compound collections, aiming to identify novel therapeutics. In the context of the Innovative Medicines Initiative consortium RESOLUTE, we developed cell-based assays for several SLCs employing a variety of scientific approaches and technologies suitable for running fully automated HTS. Here, we describe the functional assays developed for five SLCs: SLC59A1 (MFSD2A), SLC59A2 (MFSD2B), SLC6A8 (CRTR), SLC9B2 (NHA2) and SLC12A2 (NKCC1). All these transporters play relevant roles in different pathological conditions, but they still lack drugs able to specifically activate or inhibit them. To address this gap, we have developed and optimized in a miniaturized format cellular assays that enable streamlined and high-throughput investigation of compound libraries. These assays offer a valuable platform for the identification of new therapeutic modulators targeting these underexplored SLCs in a fast and efficient manner. - Source: PubMed
Publication date: 2026/08/26
Sassone FrancescaKoch JosefinaBatoulis HelenaTremolada SaraRicci FernandaMaresca GiovannaEhrmann AlexanderScarabottolo Lia - Venous thromboembolism (VTE) includes deep vein thrombosis (DVT) and pulmonary embolism (PE), the latter of which often originates from DVT and can be fatal. - Source: PubMed
Publication date: 2026/07/27
Lozano-Esparza SusanaShakt Gabrielle EBrody Jennifer AMartinez-Perez AngelConomos Matthew PGermain MarineClapham Katharine RTeder-Laving Marisvan Hylckama Vlieg AstridKauko AnniThibord FlorianBezerra Ohanna C LNadkarni Girish NMunsch GaëlleNøst Therese HaugdahlGoode Ellen LJi YuekaiChasman Daniel IReiner Alexander PTurman ConstanceWiggins Kerri LSitlani Colleen MSouto Juan CarlosLutsey Pamela LBellomo TiffanyBiobank EstonianProgram Million VeteranLi-Gao RuifangWinstén Aleksi KristianChen Ming-HueiDo RonGourhant LénaickHveem KristianArmasu Sebastian MSaut NoémiePankratz NathanGiulianini FrancoHaessler JeffreySong MingyangOlaso RobertBoerwinkle EricDochtermann DanielSoria Jose ManuelRich Stephen SSmadja DavidKoyama SatoshiRosendaal Frits RNiiranen TeemuGagnon FranceVy Ha My TZakai NeilLemarie CatherineSkogholt Anne HeidiDeleuze Jean-FrançoisPankow James SRidker Paul MLiu YuxiRice Kenneth MPyarajan SaijuCushman MaryEmmerich JospehPsaty Bruce MNatarajan PradeepJohnson Andrew DRodger Marc ASuchon PierreCouturaud FrancisMorange Pierre-EmmanuelTang WeihongKooperberg CharlesKabrhel ChristopherSabater-Lleal MariaTrégouët David-AlexandreWolberg Alisa SDamrauer Scott MSmith Nicholas L - Prenatal ethanol (alcohol) exposure (PreEE) results in abnormal tangential migration of medial ganglionic eminence (MGE)-derived GABAergic interneurons (GINs) in the embryonic mouse medial prefrontal cortex (mPFC); later in life, this is associated with impaired behavioral flexibility commonly seen in fetal alcohol spectrum disorders (FASD). The PreEE-induced abnormal tangential migration involves, in part, ethanol potentiating GABA receptor-mediated depolarization, the latter due to elevated intracellular chloride sustained primarily by the Na-K-Cl cotransporter NKCC1 in embryonic GINs. We previously reported that coincident administration of the NKCC1 antagonist bumetanide with PreEE prevents the PreEE-induced aberrant migration of GINs in the mPFC. However, such simultaneous dispensing rarely occurs in real life. In this light, the present study assessed whether bumetanide administered after PreEE mitigates the PreEE-induced aberrant tangential migration. - Source: PubMed
Koc BetulSkorput Alexander G JYeh Pamela W LYeh Hermes H