SQSTM1 Antibody (N-term S24)
- Known as:
- SQSTM1 Antibody (N-terminus S24)
- Catalog number:
- AP19120a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (N-term S24)
Related genes to: SQSTM1 Antibody (N-term S24)
- Gene:
- CHMP3 NIH gene
- Name:
- charged multivesicular body protein 3
- Previous symbol:
- VPS24
- Synonyms:
- NEDF, CGI-149
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2014-11-19
- Gene:
- HSPA4 NIH gene
- Name:
- heat shock protein family A (Hsp70) member 4
- Previous symbol:
- -
- Synonyms:
- HS24/P52, HSPH2
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-26
- Date modifiied:
- 2015-11-19
- Gene:
- KLRK1 NIH gene
- Name:
- killer cell lectin like receptor K1
- Previous symbol:
- D12S2489E
- Synonyms:
- NKG2D, KLR, NKG2-D, CD314
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- MRPS24 NIH gene
- Name:
- mitochondrial ribosomal protein S24
- Previous symbol:
- -
- Synonyms:
- MRP-S24, HSPC335
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2016-10-05
- Gene:
- RNA5SP24 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 24
- Previous symbol:
- RN5S24
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- pseudogene
- Date approved:
- 2011-08-08
- Date modifiied:
- 2012-08-07
Related products to: SQSTM1 Antibody (N-term S24)
Related articles to: SQSTM1 Antibody (N-term S24)
- Source: PubMed
- Autophagy-modulating dermatological interventions include topical, intralesional and systemic therapies, defined bioactive molecules and nutraceutical candidates. Their effects are commonly evaluated using tissue-averaged LC3-II, p62/SQSTM1 and canonical pathway markers. Although these measures support assessment of autophagy pathway engagement, they may miss spatially restricted pharmacodynamic non-response and cannot determine whether persistent local dysfunction reflects inadequate exposure or biology-limited non-response. Here we propose spatial autophagy failure (SAF) as a spatial pharmacodynamic endpoint for autophagy-targeted dermatological interventions. SAF denotes contiguous skin domains showing evidence of impaired autophagic processing and lysosomal dysfunction relative to adjacent tissue. We use photoaged skin and melanophagy as the principal test case. In this setting, persistent hyperpigmented hotspots may partly reflect localized defects in melanosome clearance alongside altered melanogenesis and melanosome transfer. Chronic wounds and pathological scars provide additional dermatological settings in which spatially heterogeneous autophagic capacity may influence treatment response. SAF assessment integrates local drug exposure, local target or pathway engagement, autophagy-lysosome readouts and phenotype maps, distinguishing exposure-limited from biology-limited non-response. Treatment effects can be quantified using total SAF burden, largest-zone size (expressed as area in two-dimensional sections or volume in three-dimensional models), zone contiguity and distance to the nearest phenotype-associated region. These SAF-zone metrics may inform lead selection, formulation and route optimization, dose and schedule selection and pharmacodynamic monitoring. Together, these measurements reframe the central questions: Does an intervention merely shift autophagy markers on average? More importantly, does adequate local exposure produce local target or pathway engagement, restore autophagic processing and improve the corresponding local phenotype? - Source: PubMed
Publication date: 2026/09/01
Lee Chang HyungLee Ki Won - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation, fibroblast-like synoviocyte hyperplasia, and progressive cartilage and bone destruction. Moxibustion is widely used as a non-pharmacological adjunctive intervention for RA; however, its specific therapeutic effects and its associations with autophagy and ferroptosis remain insufficiently characterized. This protocol describes a randomized, controlled, assessor-blinded preclinical study designed to evaluate moxibustion in a disease-syndrome combination rat model of RA. Eligible rats will undergo exposure to a controlled wind-, cold-, and dampness-related environment followed by Complete Freund's Adjuvant (CFA) injection. After successful model induction has been confirmed using prespecified criteria, animals will be randomly allocated to a normal control group, an untreated model group, a heat-matched sham-moxibustion group, a Zusanli (ST36) moxibustion group, and a methotrexate active-comparator group. All animals will undergo standardized handling and restraint procedures. Moxibustion will be administered for 20 min once daily for 15 consecutive days, whereas methotrexate will be administered at the prespecified dose and frequency. The primary outcome will be the histopathological synovitis score. Secondary outcomes will include paw volume, arthritis index, joint structural damage, serum and synovial inflammatory mediators, and functional assessments. Autophagy will be evaluated using LC3-II/LC3-I, SQSTM1/p62, Beclin-1, and complementary assessments of autophagic flux. Ferroptosis-related outcomes will include GPX4, SLC7A11, ACSL4, lipid peroxidation, glutathione, reactive oxygen species, and tissue iron levels. Outcome assessment and statistical analysis will be performed by investigators blinded to group allocation. This study is expected to provide a reproducible framework for distinguishing the specific effects of moxibustion from non-specific heat, restraint, and handling effects, and to generate mechanistic evidence supporting subsequent translational and clinical investigations. - Source: PubMed
Publication date: 2026/08/17
Sang JiajiaJin ZixiangZuo HuiZeng LongYue YiWang MengHu JunHao Feng - Neurotrophic tropomyosin receptor kinase () fusion is one of the druggable driver genes of thyroid cancer, which is confirmed in surgical specimens. However, there is a risk that certain fusion patterns may not be detected using gene panel testing. This study aimed to identify patients harboring fusion who might be overlooked by panel testing. - Source: PubMed
Toda SojiKasajima RikaOkubo YoichiroSaito NaoKadoya MeiMatsui A ISato ShinyaYamazaki HaruhikoSuganuma NobuyasuMasudo KatsuhikoSaito AyaHoshino Daisuke - The exact initiating causes of Alzheimer's disease (AD) remain inconclusive. Meanwhile, the causal sequence and interactions within its pathological network are still poorly understood, which limits the efficacy of single treatment strategies and impedes drug development. Oxidative stress, identified as a central intersection point within this network, drives the deposition of amyloid-β protein, excessive tau phosphorylation, neuroinflammation, and mitochondrial damage, creating a self-perpetuating cycle. Consequently, oxidative stress has become a focal point for multi-target interventions. This review systematically investigates the evidence of terpenoids in cellular and animal models, elucidating their protective effects via a dual antioxidant mechanism. Firstly, terpenoids activate the Keap1/Nrf2/ARE pathway, leading to the upregulation of antioxidant genes and reduced free radical generation. Secondly, they enhance PINK1/Parkin-mediated mitophagy, facilitating the clearance of damaged organelles and preventing the release of reactive oxygen species. The review also delves into the positive feedback regulatory network involving molecules like Nrf2 and key proteins of mitophagy, such as p62/SQSTM1, offering a detailed mechanistic insight into the synergistic effects of terpenoids. This study underscores the significance of natural terpenoids, with their unique regulatory role in oxidative stress, as a promising candidate library for Alzheimer's drug development due to their diverse structures, clear mechanisms, and high safety profile. Additionally, it establishes a theoretical and experimental basis for the development of novel intervention strategies targeting multiple pathways with a single drug. - Source: PubMed
Publication date: 2026/08/31
Zhang WantingWang ShanGou Xingchun