Ask about this productRelated genes to: HOOK1 antibody
- Gene:
- HOOK1 NIH gene
- Name:
- hook microtubule tethering protein 1
- Previous symbol:
- -
- Synonyms:
- HK1
- Chromosome:
- 1p32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-25
- Date modifiied:
- 2016-07-14
Related products to: HOOK1 antibody
Related articles to: HOOK1 antibody
- To establish a doxorubicin (DOX)-resistant acute myeloid leukemia (AML) cell line and explore the mechanisms of its drug resistance. - Source: PubMed
Feng Lu-LuWang Yu-TingHuang Chao-FanSun Cong-YongJun Ya-LiZhang Li - Microtubule-based organelle transport is essential for organelle positioning within cells and defines the architecture and function of highly polarized cells, like animal neurons and fungal hyphae. Early endosome transport depends on kinesin-3 motors and on cytoplasmic dynein, which binds to this organelle via Hook adaptor proteins. In filamentous fungi, these proteins can propel the indirect transport of additional organelles that hitchhike on early endosomes, like peroxisomes. However, early endosomes carry different cargoes in different fungi, and the contribution of these systems to the subcellular organization of different polarized cells is unclear. Here, we analyzed the function of the kinesin-3 motor KIN2 and of the HOOK1 adaptor in the model fungus Podospora anserina. We found that hyphal growth and morphogenesis require KIN2 and HOOK1, and that early endosome, peroxisome, vacuole, endoplasmic reticulum and mitochondrial motility depends on microtubules. We show that KIN2 and HOOK1 are required for mitochondrial localization at the sites of polarized cell growth, and for the polarized arrangement of the endoplasmic reticulum and vacuoles. Both proteins are required for the bidirectional transport of early endosomes and peroxisomes, but they differently affect their distribution. We found that KIN2 associates with some peroxisomes, and observed a low frequency of peroxisome-early endosome co-transport. Finally, we show that the GTPase RAB5B is required for the distribution and motility of early endosomes but not of peroxisomes, suggesting independent transport systems for these organelles in P. anserina. Our findings reveal a major role for KIN2 and HOOK1 in organelle dynamics during polarized cell growth. - Source: PubMed
Publication date: 2026/07/29
Hernández-Sánchez FernandoPardo-Fermín Yovanna ASchroder SaraFrutis-Osorio FernandaBrun SylvainPeraza-Reyes Leonardo - Peripheral nerve injury (PNI) represents a prevalent clinical condition, often resulting from mechanical trauma or tumor resection, which frequently induces persistent sensory deficits, motor impairment, neuropathic pain, or paralysis. Consequently, substantial socioeconomic burdens are imposed on affected individuals. Autologous nerve transplantation is often considered the preferred approach for reconstructing peripheral nerve defects; however, this technique is associated with limitations including donor-site sensory loss, restricted graft length, and nerve mismatches. Recently, peripheral blood mononuclear cells (PBMCs) have emerged as a focal point in nerve regeneration research due to their accessibility, immunomodulatory properties, and neuro-reparative potential. Nevertheless, the precise mechanisms underlying PBMC-mediated nerve repair remain incompletely characterized, and their molecular pathways require further elucidation. This study explores the potential role of PBMCs in promoting peripheral nerve regeneration, with a particular focus on their regulation of retrograde brain-derived neurotrophic factor (BDNF) transport through modulation of Hook1 expression and associated molecular pathways. This research seeks to provide novel insights for PBMC-based therapeutic strategies and establish a theoretical foundation for clinical translation. Implementation challenges and translational prospects for PBMCs in nerve regeneration are also critically evaluated. - Source: PubMed
Publication date: 2025/08/07
Chen YiWen YubinZhang MingyueNie JingSun Guangfeng Introduction: Accumulation of fat in omental visceral adipose tissue (OVAT) is strongly linked to metabolic diseases. Our recent findings show a distinct and more accessible chromatin landscape of the visceral depot compared to its subcutaneous counterpart. Based on integrated analysis of chromatin accessibility and transcriptomics, we identified previously unrecognised genes linked with obesity. Here, we performed in-depth analyses of one of the candidates, HOOK1, and tested for depot-specific gene expression, correlation with clinical traits and regulatory mechanisms including DNA methylation. - Source: PubMed
Publication date: 2025/07/25
Svensson Stina Ingrid AliceSaeed SadiaHoffmann AnneGhosh AdhidebWolfrum ChristianDahl Mai BrittCayir AkinRønningen TorunnBai BaoyanMala TomKristinsson Jon AdalsteinKovacs PeterBlüher MatthiasValderhaug Tone GretlandBöttcher Yvonne
- Oligoasthenoteratozoospermia (OAT) is a prevalent situation of male infertility partly caused by genetic defects with largely undiscovered. To further unravel the genetic etiology of OAT, we recruited cases for whole-exome sequencing (WES) to screen candidate pathogenic mutations. Here, we identified a heterozygous missense mutation in transcription factor-like 5 (TCFL5) (NM_006602.4: c.1207G > A: p.E403K) from two infertile brothers born into a non-consanguineous family. TCFL5 was previously linked to male infertility since Tcfl5 male mice manifested infertile due to OAT, while Tcfl5 mice could not be generated. Sperm morphological analysis of these brothers exhibited a similar OAT phenotype to Tcfl5 mice. In vitro functional analysis performed to explore the pathogenicity of TCFL5 mutation. Regardless of no significant effect on the expression of mutant TCFL5 detected by western blotting and immunofluorescence, dual-luciferase reporter assay revealed a serious impact on its transcriptional regulatory function. Many crucial genes involved in spermatogenesis, such as DMRT1, DAZL, SYCE1, SPACA1, CNTROB, IFT88, HOOK1 and SPATA6, occurred transcriptional abnormalities after TCFL5 mutated. Our results showed that TCFL5 mutation disrupted the normal transcription of spermatogenesis genes, finally resulting in male infertility raised by OAT. Our work firstly linked TCFL5 mutation to male infertility in human, which provides a new perspective on the genetic underpinnings of OAT and a theoretical basis for clinic genetic counseling and treatment strategies selection. - Source: PubMed
Publication date: 2025/07/25
Yu KexinZhang WenchenWang YuXiang MingfeiZheng NaZhang JingjingZha XiaominDuan ZongliuWang FengsongCao YunxiaZhu Fuxi