SLC12A2 Antibody
- Known as:
- SLC12A2 Antibody
- Catalog number:
- XW-8139
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- 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
- Lymphedema is a chronic condition characterized by the accumulation of fluid due to impaired lymphatic drainage, frequently occurring secondary to chronic venous insufficiency (CVI), malignancy, or obesity. Despite known environmental and clinical risk factors, the genetic contributors to lymphedema and CVI have been understudied. - Source: PubMed
Publication date: 2026/04/22
Peloso Gina MAdhikari NimishYoung Melissa MCho KellyKinlay Scott - Colorectal cancer (CRC) remains a leading cause of cancer‑related morbidity and mortality worldwide. Although the adenoma-carcinoma sequence and its genetic drivers are well described, the earliest cellular and molecular events initiating tumorigenesis within histologically normal colonic epithelium remain poorly defined. This study aims to identify tumor‑initiating cells (TICs), distinguish them from normal stem‑like cells (nSTMs), and delineate early transcriptional and signaling programs using single‑cell RNA sequencing (scRNA‑seq) from paired normal‑appearing and transformed human colonic tissues. - Source: PubMed
Publication date: 2026/03/27
Jaiswal SangeetaThe StephanieChang Tse-ShaoShi JiaqiWang Thomas D - Colorectal cancer (CRC) is the thirdmost common cancer and a leading cause of cancer deaths worldwide, with over 1.9 million cases diagnosed in 2022. Due to poor response to classical cancer treatments, CRC is associated with low survival rates. This creates an urgent need for better understanding of CRC pathology. Cell death occurs continuously in solid tumors, and is also induced acutely, during chemotherapy. Dead cells are cleared by phagocytes via 'efferocytosis', an anti-inflammatory process that can lead to immune escape and reduced therapeutic efficacy. We hypothesized that efferocytosis might contribute to tumor development and that manipulating this process could be beneficial for CRC therapy. - Source: PubMed
Publication date: 2026/03/09
Boeckaerts LauraAaes Tania LøveScheirlinckx EviChoi Sze MenIncik YunusGonçalves AmandaHochepied TinoVereecke LarsRavichandran Kodi S - Stress promotes the progression from borderline hypertension to sustained hypertension, but the mechanism remains unclear. We investigated the role of corticotropin-releasing factor (CRF)-expressing neurons in the central nucleus of amygdala (CeA) on arterial blood pressure (ABP) and sympathetic activity of borderline hypertensive rats (BHRs) subjected to chronic unpredictable mild stress (CUMS). CUMS induced sustained hypertension, and led to increased delta-FosB expression as well as enhanced spontaneous and evoked firing of CeA CRF-expressing neurons in BHRs. Furthermore, optogenetic activation of CeA CRF-expressing neurons significantly increased the sympathetic outflow and ABP in BHRs. Impaired GABAergic inhibition, a depolarizing shift of GABA reversal potential (EGABA), disrupted chloride homeostasis and increased NKCC1 expression were observed in CeA CRF-expressing neurons in BHRs subjected to CUMS. NKCC1 inhibition with bumetanide restored GABAergic inhibition and chloride homeostasis, normalized neuronal excitability, leading to reduced sympathetic vasomotor tone in CUMS BHRs. These results indicate that NKCC1-mediated disruption of chloride homeostasis in CeA CRF-expressing neurons contributes to elevated sympathetic activity and hypertension under chronic stress. These findings enhance our understanding of the neuronal and molecular mechanisms underlying stress-induced hypertension and reveal potential targets for its prevention and treatment. - Source: PubMed
Publication date: 2026/03/16
Ma HongyuZhang YingGuo XinqiZhao QiyueYang PeiyunLiu YanGuan YueWei YanMa Huijie - Here, we recount the story of a remarkable young girl who demonstrated extraordinary courage and resilience while confronting significant health challenges over the span of 23 years. Her journey is a testament to her determination to survive and thrive despite overwhelming obstacles. We detail the investigative efforts aimed at associating her clinical symptoms with a specific membrane transporter: the Na-K-2Cl cotransporter-1 (NKCC1), which this laboratory has dedicated more than three decades to studying. The work summarized here covers experiments using patient-derived cells, cells engineered to express wild-type or mutant cotransporter, and genetically modified mice carrying this patient-specific alteration. It is illuminated by reports of other rare human deleterious mutations, and work done by us and others using NKCC1 knockout mouse models. During our studies, we uncovered details regarding the trafficking of NKCC1, shedding light on how the protein is transported and positioned to carry out its function in epithelial cells. Furthermore, our findings revealed that NKCC1 may play a role in energy metabolism, suggesting that its activity influences metabolic processes within affected tissues. Our investigations also underscored the involvement of NKCC1 in the development of the nervous system. In addition, we discuss the evidence found that intestinal dysfunction is linked to NKCC1 abnormalities and evidence showing an established link between the cotransporter and epithelial cell-mediated inflammation. This patient's story stands as a testament to perseverance and the importance of scientific inquiry in understanding rare genetic disorders. - Source: PubMed
Publication date: 2026/03/11
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