DYNLT3

Last update 08 May 2025

Basic Info

Synonyms

dynein light chain Tctex-type 3, DYNLT3, Protein 91/23

+ [4]

Introduction

Acts as one of several non-catalytic accessory components of the cytoplasmic dynein 1 complex that are thought to be involved in linking dynein to cargos and to adapter proteins that regulate dynein function. Cytoplasmic dynein 1 acts as a motor for the intracellular retrograde motility of vesicles and organelles along microtubules. Probably binds BUB3 as part of transport cargo. Required for the efficient progression through mitosis (By similarity).

100 Clinical Results associated with DYNLT3

100 Translational Medicine associated with DYNLT3

0 Patents (Medical) associated with DYNLT3

Literatures (Medical) associated with DYNLT3

01 Sep 2023·The Journal of biological chemistry

Alternative splicing regulates adaptor protein binding, trafficking, and activity of the Vps10p domain receptor SorCS2 in neuronal development.

Article

Author: Voss, Lasse Frank ; Madsen, Peder ; Sander, Marie Rubin ; Bentsen, Andreas Høiberg ; Fuglsang, Marie ; Glerup, Simon ; Skeldal, Sune ; Gustafsen, Camilla ; Buttenschøn, Henriette ; Mølgaard, Simon ; Kaas, Mathias ; Lende, Jonas ; Pedersen, Sarah Broholt ; Demange, Perline

The Vps10p domain receptor SorCS2 is crucial for the development and function of the nervous system and essential for brain-derived neurotrophic factor (BDNF)-induced changes in neuronal morphology and plasticity. SorCS2 regulates the subcellular trafficking of the BDNF signaling receptor TrkB as well as selected neurotransmitter receptors in a manner that is dependent on the SorCS2 intracellular domain (ICD). However, the cellular machinery and adaptor protein (AP) interactions that regulate receptor trafficking via the SorCS2 ICD are unknown. We here identify four splice variants of human SorCS2 differing in the insertion of an acidic cluster motif and/or a serine residue within the ICD. We show that each variant undergoes posttranslational proteolytic processing into a one- or two-chain receptor, giving rise to eight protein isoforms, the expression of which differs between neuronal and nonneuronal tissues and is affected by cellular stressors. We found that the only variants without the serine were able to rescue BDNF-induced branching of SorCS2 knockout hippocampal neurons, while variants without the acidic cluster showed increased interactions with clathrin-associated APs AP-1, AP-2, and AP-3. Using yeast two-hybrid screens, we further discovered that all variants bound dynein light chain Tctex-type 3; however, only variants with an acidic cluster motif bound kinesin light chain 1. Accordingly, splice variants showed markedly different trafficking properties and localized to different subcellular compartments. Taken together, our findings demonstrate the existence of eight functional SorCS2 isoforms with differential capacity for interactions with cytosolic ligands dynein light chain Tctex-type 3 and kinesin light chain 1, which potentially allows cell-type specific SorCS2 trafficking and BDNF signaling.

01 Jul 2023·Cancer medicine

The role of DYNLT3 in breast cancer proliferation, migration, and invasion via epithelial-to-mesenchymal transition.

Article

Author: Zhu, Xueqiong ; Wang, Han ; Liu, Tingxian ; Chen, Xin ; Song, Yizuo ; Zhu, Xuejie ; Jin, Yanshan

PURPOSEDYNLT3 is identified as an age-related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis.METHODSThe differential expression of DYNLT3 among breast cancer, breast fibroids, and normal tissues, as well as in various breast cancer cell lines were detected by immunohistochemical staining, real-time quantitative reverse transcription-PCR and Western blotting, respectively. Additionally, the role of DYNLT3 on cell viability and proliferation were observed through cell counting kit-8, bromodeoxyuridine, and colony formation experiments. Migratory and invasive abilities was envaulted by wound healing and Transwell methods. Apoptotic cells rate was examined by flow cytometry. Furthermore, nude mice xenograft models were established to confirm the role of DYNLT3 in tumor formation in vivo.RESULTSDYNLT3 expression was highly rising in both breast cancer tissues and cells. DYNLT3 knockdown obviously suppressed cell growth, migration and invasion, and induced cell apoptosis in MDA-MB-231 and MCF-7 breast cancer cells. The overexpression of DYNLT3 exerted the opposite effect in MDA-MB-231 cells. Moreover, DYNLT3 knockdown inhibited tumor formation in vivo. Mechanistically, an elevation of N-cadherin and vimentin levels and a decline of E-cadherin were observed when DYNLT3 was upregulated, which was reversed when DYNLT3 knockdown was performed.CONCLUSIONDYNLT3 may function as a tumor-promotor of age-associated breast cancer, which is expected to provide experimental basis for new treatment options.

01 Dec 2020·Breast Cancer ResearchQ1 · MEDICINE

Age-associated genes in human mammary gland drive human breast cancer progression

Q1 · MEDICINE

ArticleOA

Author: Lai, Zhao ; Huang, Tim H-M ; Sun, Lu-Zhe ; Zhu, Haiyan ; Michalek, Joel E ; Zhou, You ; Chen, Yidong ; Gu, Xiang ; Houghton, Peter ; Wang, Bingzhi ; Horning, Aaron M

AbstractBackgroundAging is a comorbidity of breast cancer suggesting that aging-associated transcriptome changes may promote breast cancer progression. However, the mechanism underlying the age effect on breast cancer remains poorly understood.MethodWe analyzed transcriptomics of the matched normal breast tissues from the 82 breast cancer patients in The Cancer Genome Atlas (TCGA) dataset with linear regression for genes with age-associated expression that are not associated with menopause. We also analyzed differentially expressed genes between the paired tumor and non-tumor breast tissues in TCGA for the identification of age and breast cancer (ABC)-associated genes. A few of these genes were selected for further investigation of their malignancy-regulating activities with in vitro and in vivo assays.ResultsWe identified 148 upregulated and 189 downregulated genes during aging. Overlapping of tumor-associated genes between normal and tumor tissues with age-dependent genes resulted in 14 upregulated and 24 downregulated genes that were both age and breast cancer associated. These genes are predictive in relapse-free survival, indicative of their potential tumor promoting or suppressive functions, respectively. Knockdown of two upregulated genes (DYNLT3 and P4HA3) or overexpression of the downregulated ALX4 significantly reduced breast cancer cell proliferation, migration, and clonogenicity. Moreover, knockdown of P4HA3 reduced growth and metastasis whereas overexpression of ALX4 inhibited the growth of xenografted breast cancer cells in mice.ConclusionOur study suggests that transcriptome alterations during aging may contribute to breast tumorigenesis. DYNLT3, P4HA3, and ALX4 play significant roles in breast cancer progression.

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DYNLT3

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