Ask about this productRelated genes to: PEPD antibody
- Gene:
- PEPD NIH gene
- Name:
- peptidase D
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-07-12
Related products to: PEPD antibody
Related articles to: PEPD antibody
- p95HER2 is commonly expressed in human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC) and is generated primarily from shedding of the extracellular domain of HER2. p95HER2 is oncogenic, driving aggressive tumor growth, and conferring drug resistance. Targeting p95HER2 is challenging. Clinically approved HER2 inhibitors either cannot bind to p95HER2 or show limited inhibitory effects. We used cell lines and orthotopic tumor models (cell line xenografts and patient derived xenografts) to investigate the effects of HER2 inhibitors on p95HER2 and other key signaling proteins in HER2-positive BC, and to compare the therapeutic activities of different HER2 inhibitors. The HER2 inhibitors represent different mechanisms of actions, including trastuzumab, pertuzumab, tucatinib, and lapatinib, all of which are clinically approved, as well as PEPD, a recombinant human protein which was previously shown to induce the degradation of HER2 and epidermal growth factor receptor (EGFR). EGFR is closely related to HER2 and is implicated in drug resistance in HER2-positive BC. HER2-positive BC cells and tumors, despite p95HER2 expression, are exquisitely sensitive to targeted degradation of HER2 and EGFR by PEPD. PEPD-induced degradation of HER2 also consistently eliminates p95HER2. PEPD is far more effective than the clinically approved HER2 inhibitors in inhibiting the oncogenic signaling and growth of HER2-positive BC cells and tumors expressing p95HER2. Most notably, in an orthotopic PDX of HER2-positive BC expressing p95HER2, which is insensitive to trastuzumab and tucatinib, PEPD achieved complete and lasting tumor elimination. Despite p95HER2 expression and resistance to current HER2 inhibitors, HER2-positive BC cells and tumors are highly vulnerable to PEPD-induced degradation of HER2 and EGFR. By inducing HER2 degradation, PEPD eliminates p95HER2 in HER2-positive BC cells and tumors. - Source: PubMed
Publication date: 2026/04/20
Yang LuBhattacharya ArupLi YunPeterson DarrellZhang Yuesheng - Prolidase deficiency is a rare autosomal recessive metabolic disorder resulting from mutations in the PEPD gene, leading to impaired collagen turnover and a broad spectrum of clinical features. Its manifestations include recurrent ulcerative skin lesions, recurrent infections, and hematological abnormalities. Celiac disease, another multisystem disorder, presents with chronic diarrhea, malabsorption, and iron deficiency anemia. The coexistence of both conditions is exceedingly rare and may lead to diagnostic delays. - Source: PubMed
Publication date: 2026/04/09
Gupta ViploveYadav VaibhavPandey Ved PrakashDubey SanjayJamra YogendraPawar Akash - This study aims to investigate the therapeutic effects of the Bushen Huatan (BSHT) Formula on non-obese polycystic ovary syndrome (PCOS) rats, and to explore its potential mechanisms of action. - Source: PubMed
Publication date: 2026/04/09
Chen MengZhang RuiyuanHuang YingPan YuxinYang JinrongHuang Yinghong - Altered tryptophan-kynurenine metabolism has been associated with schizophrenia. Beyond healthy-control differences, elevated brain kynurenic acid and reduced peripheral metabolites have been linked to symptoms and cognitive deficits. Nonetheless, exercise has been shown to rebalance this pathway by enhancing peripheral kynurenine turnover, with no clear evidence yet in schizophrenia. - Source: PubMed
Publication date: 2026/03/16
Rißmayer MatthiasFischer JuliaHanssen RuthKretschmer Alina ChloéBlaschke Stefan JJelic SofijaAnnas SophiaRihm AlinaMarkser AnnaKrombholz SophiaThevis MarioHohmann ChristopherSchönau EckhardHokamp Nils GroßeBloch WilhelmKambeitz JosephJavelle FlorianLichtenstein Theresa - Metabolites serve not only as metabolic intermediates but also as potent signaling molecules that orchestrate cell fate. However, decoding the specific "metabolite-target-phenotype" axis within complex pathophysiological environment remains a major challenge due to the lack of systematic target deconvolution strategies. Here, we developed Circulating Metabolite-Target Responsive Accessibility Profiling (CM-TRAP), an integrated multi-omics workflow that couples untargeted metabolomic screening with TRAP-based chemical proteomic target discovery. This analytical framework enables the direct linkage of disease characteristic metabolic alterations to their molecular targets. - Source: PubMed
Publication date: 2026/03/05
Wang XinmiaoHe XiangyuPu XiaoyuYang XingchaoLi YiZhang HanqingHao HaipingShao ChangYe Hui