Ask about this productRelated genes to: ACTR3B Blocking Peptide
- Gene:
- ACTR3B NIH gene
- Name:
- actin related protein 3B
- Previous symbol:
- -
- Synonyms:
- ARP11, ARP3beta
- Chromosome:
- 7q36.1-q36.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-19
- Date modifiied:
- 2019-01-10
Related products to: ACTR3B Blocking Peptide
Related articles to: ACTR3B Blocking Peptide
- Endocrine therapy (ET) selection in estrogen receptor-positive breast cancer (ER + BC) is guided by menopausal status and tolerability rather than tumor biology, despite substantial heterogeneity in recurrence. We hypothesized that baseline gene expression differentially associates with recurrence depending on initial ET class. In a retrospective cohort of 74 ER+/HER2- patients treated with adjuvant ET, we profiled baseline tumor RNA and fitted adjusted Cox models for gene and ET interactions on time-to-recurrence and time-to-switch. Among selective estrogen receptor modulators-initiated patients, higher expression of , , , , and was associated with markedly increased recurrence, while no comparable association was observed among aromatase inhibitors-initiated patients. Forty-one percent of patients switched ET at least once, predominantly due to intolerance (joint pain, unspecified side effects); switching was not consistently associated with tumor biology. These hypothesis-generating findings identify candidate gene and ET interactions and motivate validation in larger, independent cohorts. - Source: PubMed
Publication date: 2026/06/30
Jones VeronicaWang YongzheQuinones ChristineAljaber DanaNelson EvaNath AritroKang IreneRugo HopeYee LisaSeewaldt VictoriaMortimer Joanne - Despite the critical role of endocytosis-related genes in oncogenic processes, research exploring their potential for prognosticating hepatocellular carcinoma (HCC) remains limited. Establishing a connection between endocytosis and HCC is imperative. This study aimed to create a gene signature related to endocytosis to identify HCC subtypes and predict outcomes. - Source: PubMed
Publication date: 2025/06/27
Zhang LitingZhou DanGao XiaoqinLi JunfengXie Xiaodong - During mammalian spermatogenesis, the cytoskeleton system plays a significant role in morphological changes. Male infertility such as non-obstructive azoospermia (NOA) might be explained by studies of the cytoskeletal system during spermatogenesis. - Source: PubMed
Publication date: 2025/01/25
Hashemi Karoii DanialAzizi HosseinDarvari MaryamQorbanee AliHawezy Dawan Jamal - Germline variants in the NSD1 gene are responsible for Sotos syndrome, while somatic variants promote neoplastic cell transformation. Our previous studies revealed three alternative RNA isoforms of present in fibroblast cell lines (FBs): the canonical full transcript and 2 alternative transcripts, termed AT2 (NSD1 Δ5Δ7) and AT3 ( Δ19-23 at the 5' end). The precise molecular pathways affected by each specific isoform of are uncharacterized to date. To elucidate the role of these isoforms, their expression was suppressed by siRNA knockdown in FBs and protein expression and transcriptome data was explored. We demonstrate that one gene target of isoform AT2 is ARP3 actin-related protein 3 homolog B (). We show that loss of both canonical and AT2 isoforms impaired the ability of fibroblasts to regulate the actin cytoskeleton, and we observed that this caused selective loss of stress fibers. Our findings provide novel insights into function by distinguishing isoform function and demonstrating an essential role of in regulating the actin cytoskeleton and stress fiber formation in fibroblasts. - Source: PubMed
Publication date: 2024/08/24
Conteduca GiuseppinaCangelosi DavideBaldo ChiaraArado AlessiaTesta BarbaraWagner Ryan TRobertson Keith DDequiedt FranckFitzsimmons LaneMalacarne MichelaFilaci GilbertoCoviello Domenico A - Cemento-ossifying fibroma (COF) of the jaws is currently classified as a benign mesenchymal odontogenic tumor, and only targeted approaches have been used to assess its genetic alterations. A minimal proportion of COFs harbor CDC73 somatic mutations, and copy number alterations (CNAs) involving chromosomes 7 and 12 have recently been reported in a small proportion of cases. However, the genetic background of COFs remains obscure. We used a combination of whole-exome sequencing and RNA sequencing to assess somatic mutations, fusion transcripts, and CNAs in a cohort of 12 freshly collected COFs. No recurrent fusions have been identified among the 5 cases successfully analyzed by RNA sequencing, with in-frame fusions being detected in 2 cases (MARS1::GOLT1B and PARG::BMS1 in one case and NCLN::FZR1 and NFIC::SAMD1 in the other case) and no candidate fusions identified for the remaining 3 cases. No recurrent pathogenic mutations were detected in the 11 cases that had undergone whole-exome sequencing. A KRAS p.L19F missense variant was detected in one case, and 2 CDC73 deletions were detected in another case. The other variants were of uncertain significance and included variants in PC, ACTB, DOK6, HACE1, and COL1A2 and previously unreported variants in PTPN14, ATP5F1C, APOBEC1, HDAC5, ATF7IP, PARP2, and ACTR3B. The affected genes do not clearly converge on any signaling pathway. CNAs were detected in 5/11 cases (45%), with copy gains involving chromosome 12 occurring in 3/11 cases (27%). In conclusion, no recurrent fusions or pathogenic variants have been detected in the present COF cohort, with copy gains involving chromosome 12 occurring in 27% of cases. - Source: PubMed
Publication date: 2023/11/22
Gomez Ricardo SantiagoEl Mouatani AhmedDuarte-Andrade Filipe FidelesPereira Thais Dos Santos FontesGuimarães Letícia MartinsGayden TenzinFaury DamienNakada Emily MLanglois SylvieSinnett Danielde Castro Wagner HenriquesDiniz Marina GonçalvesJabado NadaGomes Carolina Cavalieri