Ask about this productRelated genes to: SLITRK6 antibody
- Gene:
- SLITRK6 NIH gene
- Name:
- SLIT and NTRK like family member 6
- Previous symbol:
- -
- Synonyms:
- FLJ22774
- Chromosome:
- 13q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-08
- Date modifiied:
- 2019-04-23
Related products to: SLITRK6 antibody
Related articles to: SLITRK6 antibody
- Nulliparity is associated with adverse pregnancy outcomes including preeclampsia, preterm birth, lower birth weight and stillbirth although mechanisms are unclear. Placental gene expression differences, which also vary by fetal sex, may drive altered placental function and explain pregnancy outcome differences between nulliparous and multiparous women. This study aims to identify placental gene expression differences based on parity and examine their relationship with birth weight. - Source: PubMed
Publication date: 2026/01/06
Haizler-Cohen LylachWang GuisongHabtewold Tesfa DejenieWijesiriwardhana PrabhaviGrantz Katherine LTekola-Ayele Fasil - Myocardial infarction (MI) and subsequent heart failure are frequently accompanied by chronic kidney disease, further impairing outcomes and complicating treatment. To better understand heart-kidney crosstalk, we used RNA sequencing data to infer interorgan signalling after experimentally induced MI in mice, focusing on secreted biomolecules and interorgan cross talk that may drive cardiorenal syndrome (CRS). To assess acute and chronic effects, we examined kidneys at 5d and 28d post-MI, evaluating changes in renal gene expression and fibrosis. During the acute phase 5d post-MI, several genes inferred to target kidney receptors were highly upregulated in the cardiac infarct zone, with Postn and Spp1 being the most probable ligands. However, only minor changes in gene expression were detected in the kidney 5d post-MI. At 28d post-MI, renal fibrosis and the number of differentially expressed genes (DEGs) in the kidney increased. Gene ontology enrichment suggested metabolic adaptions as part of a long-term response. Based on upregulated DEGs in kidney 28d post-MI, we suggest two kidney-to-heart interactions: Slitrk6-Ptprs and Gdf15-Tgfbr2. In vitro, GDF-15 treatment of human cardiac fibroblasts induced pro-fibrotic gene expression, mirroring in vivo changes in the heart. Our data suggest that MI in mice elicits minimal acute response in kidney but triggers chronic transcriptional and pro-fibrotic changes in kidney, potentially driven by altered renal metabolism. The inference of interorgan signalling molecules such as GDF-15 points towards candidate mediators of CRS and provides a basis for future mechanistic and clinical studies. - Source: PubMed
Publication date: 2025/12/05
Wolf HannaKupsch SvenjaHaacke Virginia KBacmeister LucasWeber SusanneHilgendorf IngoKeller TillDechend RalfHuber Tobias BWestermann DirkLindner Diana - Chronic obstructive pulmonary disease (COPD) is a leading challenge of global public health that predominantly affects developing countries. Although smoking is the main risk factor, only a fraction of smokers develop COPD. This study aimed to identify biomarkers or therapeutic targets that would effectively aid early diagnosis and treatment of smoking-induced COPD. - Source: PubMed
Publication date: 2025/08/01
Mokaram Doust Delkhah ArmanGhazvini AliArabfard Masoud - Antibody drug conjugates represent a promising class of antineoplastic agents comprised of a monoclonal antibody linked to a potent cytotoxic payload for targeted delivery of chemotherapy to tumors. Various antibody drug conjugates have demonstrated impressive efficacy in patients with metastatic urothelial carcinoma in clinical trials, leading to two FDA approved therapies and several other agents and combinations in clinical development. - Source: PubMed
Publication date: 2024/03/12
Grant Michael JStockhammer PaulAustin Matthew RNemeth ZsuzsannaPetrylak Daniel P - Circulating proteins may provide insights into the varying biological mechanisms involved in heart failure (HF) with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). We aimed to identify specific proteomic patterns for HF, by comparing proteomic profiles across the ejection fraction spectrum. We investigated 4210 circulating proteins in 739 patients with normal (Stage A/Healthy) or elevated (Stage B) filling pressures, HFpEF, or ischemic HFrEF (iHFrEF). We found 2122 differentially expressed proteins between iHFrEF-Stage A/Healthy, 1462 between iHFrEF-HFpEF and 52 between HFpEF-Stage A/Healthy. Of these 52 proteins, 50 were also found in iHFrEF vs. Stage A/Healthy, leaving SLITRK6 and NELL2 expressed in lower levels only in HFpEF. Moreover, 108 proteins, linked to regulation of cell fate commitment, differed only between iHFrEF-HFpEF. Proteomics across the HF spectrum reveals overlap in differentially expressed proteins compared to stage A/Healthy. Multiple proteins are unique for distinguishing iHFrEF from HFpEF, supporting the capacity of proteomics to discern between these conditions. - Source: PubMed
Publication date: 2024/06/27
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