INCENP

Last update 23 Jan 2025

Basic Info

Synonyms

FLJ31633, INCENP, inner centromere protein

Introduction

Component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Acts as a scaffold regulating CPC localization and activity. The C-terminus associates with AURKB or AURKC, the N-terminus associated with BIRC5/survivin and CDCA8/borealin tethers the CPC to the inner centromere, and the microtubule binding activity within the central SAH domain directs AURKB/C toward substrates near microtubules (PubMed:15316025, PubMed:12925766, PubMed:27332895). The flexibility of the SAH domain is proposed to allow AURKB/C to follow substrates on dynamic microtubules while ensuring CPC docking to static chromatin (By similarity). Activates AURKB and AURKC (PubMed:27332895). Required for localization of CBX5 to mitotic centromeres (PubMed:21346195). Controls the kinetochore localization of BUB1 (PubMed:16760428).

100 Clinical Results associated with INCENP

100 Translational Medicine associated with INCENP

0 Patents (Medical) associated with INCENP

326

Literatures (Medical) associated with INCENP

17 Dec 2024·Medical Review

MST1 interactomes profiling across cell death in esophageal squamous cell carcinoma

Article

Author: Wu, Yueguang ; Zhang, Weimin ; Zhou, Yan ; Liu, Huijuan ; Cui, Yongping ; Gao, Mingwei ; Song, Qiqin ; Zhuang, Xuehan ; Zhang, Li ; Bi, Shanshan

AbstractObjectivesResistance to apoptosis in esophageal squamous cell carcinoma (ESCC) constitutes a significant impediment to treatment efficacy. Exploring alternative cell death pathways and their regulatory factors beyond apoptosis is crucial for overcoming drug resistance and enhancing therapeutic outcomes in ESCC.MethodsMammalian Ste 20-like kinase 1 (MST1) is implicated in regulating various cell deaths, including apoptosis, autophagy, and pyroptosis. Employing enhanced ascorbate peroxidase 2 (APEX2) proximity labeling coupled with immunoprecipitation-mass spectrometry (IP-MS), we elucidated the interactomes of MST1 across these three cell death paradigms.ResultsProteomic profiling unveiled the functional roles and subcellular localization of MST1 and its interacting proteins during normal proliferation and various cell death processes. Notably, MST1 exhibited an expanded interactome during cell death compared to normal proliferation and chromosome remodeling functions consistently. In apoptosis, there was a notable increase of mitosis-associated proteins such as INCENP, ANLN, KIF23, SHCBP1 and SUPT16H, which interacted with MST1, alongside decreased expression of the pre-apoptotic protein STK3. During autophagy, the bindings of DNA repair-related proteins CBX8 and m6A reader YTHDC1 to MST1 were enhanced. In pyroptosis, LRRFIP2 and FLII which can inhibit pyroptosis increasingly binding to MST1.ConclusionsOur findings delineate potential mechanisms through which MST1 and its interactomes regulate cell death, paving the way for further investigation to validate and consolidate these observations.

11 Dec 2024·mBio

On the possibility of yet a third kinetochore system in the protist phylum Euglenozoa

Article

Author: Raas, Maximilian W. D. ; Tromer, Eelco C. ; Faktorová, Drahomíra ; Lukeš, Julius ; Akiyoshi, Bungo ; Tripathi, Pragya ; Benz, Corinna

ABSTRACT Transmission of genetic material from one generation to the next is a fundamental feature of all living cells. In eukaryotes, a macromolecular complex called the kinetochore plays crucial roles during chromosome segregation by linking chromosomes to spindle microtubules. Little is known about this process in evolutionarily diverse protists. Within the supergroup Discoba, Euglenozoa forms a speciose group of unicellular flagellates—kinetoplastids, euglenids, and diplonemids. Kinetoplastids have an unconventional kinetochore system, while euglenids have subunits that are conserved among most eukaryotes. For diplonemids, a group of extremely diverse and abundant marine flagellates, it remains unclear what kind of kinetochores are present. Here, we employed deep homology detection protocols using profile-versus-profile Hidden Markov Model searches and AlphaFold-based structural comparisons to detect homologies that might have been previously missed. Interestingly, we still could not detect orthologs for most of the kinetoplastid or canonical kinetochore subunits with few exceptions including a putative centromere-specific histone H3 variant (cenH3/CENP-A), the spindle checkpoint protein Mad2, the chromosomal passenger complex members Aurora and INCENP, and broadly conserved proteins like CLK kinase and the meiotic synaptonemal complex proteins SYCP2/3 that also function at kinetoplastid kinetochores. We examined the localization of five candidate kinetochore-associated proteins in the model diplonemid, Paradiplonema papillatum. Pp CENP-A shows discrete dots in the nucleus, implying that it is likely a kinetochore component. Pp Mad2, Pp CLK KKT10/19 , Pp SYCP2L1 KKT17/18 , and Pp INCENP reside in the nucleus, but no clear kinetochore localization was observed. Altogether, these results point to the possibility that diplonemids evolved a hitherto unknown type of kinetochore system. IMPORTANCEA macromolecular assembly called the kinetochore is essential for the segregation of genetic material during eukaryotic cell division. Therefore, characterization of kinetochores across species is essential for understanding the mechanisms involved in this key process across the eukaryotic tree of life. In particular, little is known about kinetochores in divergent protists such as Euglenozoa, a group of unicellular flagellates that includes kinetoplastids, euglenids, and diplonemids, the latter being a highly diverse and abundant component of marine plankton. While kinetoplastids have an unconventional kinetochore system and euglenids have a canonical one similar to traditional model eukaryotes, preliminary searches detected neither unconventional nor canonical kinetochore components in diplonemids. Here, we employed state-of-the-art deep homology detection protocols but still could not detect orthologs for the bulk of kinetoplastid-specific nor canonical kinetochore proteins in diplonemids except for a putative centromere-specific histone H3 variant. Our results suggest that diplonemids evolved kinetochores that do not resemble previously known ones.

01 Nov 2024·Urologic Oncology: Seminars and Original Investigations

Genetic variations related to the prostate cancer risk: A field synopsis and revaluation by Bayesian approaches of genome-wide association studies

Article

Author: de Oliveira, Ana Carolina Alves ; Monteiro, José Rogério Souza ; Pereira, Adenilson Leão ; Dos Santos, Naum Neves da Costa ; da Silva, Jonatan Pinho Rodrigues ; Monteiro, André Victor Oliveira ; Brasileiro, Samuel Arcebispo ; Botelho, Juliana Campos ; Sobreira, Luis Eduardo Rodrigues ; Leal, Alessandro Luiz Araújo Bentes ; da Silva, Felipe Rodolfo Pereira

Prostate cancer (PCa) is a complex disease influenced by many factors, with the genetic contribution for this neoplasia having a great role in its risk. The literature brings an increased number of Genome-Wide Association Studies (GWAS's) that attempt to elucidate the genetic associations with PCa. However, these genome studies have a considerable rate of false-positive data whose results may be biased. Therefore, we aimed to apply Bayesian approaches on significant associations among polymorphisms and PCa from GWAS's data. A literature search was performed for data published before April 20, 2024, whereby two investigators used a specific combination of keywords and Boolean operators in the search ("prostate carcinoma or prostate cancer or PCa" and "polymorphism or genetic variation" and "Genome-Wide Association Study or GWAS"). The records were retrieved, and the data were extracted with further application of two different Bayesian approaches: The False Positive Report Probability (FPRP) and the Bayesian False-Discovery Probability (BFDP), both at the prior probabilities of 10^-3 and 10^-6. The data were considered as noteworthy at the level of FPRP <0.2 and BFDP <0.8. Besides, in-silico analyses by gene-gene network and gene enrichment were performed to evaluate the role of the noteworthy genes in PCa. As results, 13 GWAS's were included, with 2,520 values for FPRP and 1,368 values for BFDP being obtained. Our study showed an extensive number of gene variations as noteworthy candidate biomarkers for PCa risk, with highlighting for those occurred in the 8q24 locus and in the MSMB, ITGA6, SUN2, FGF10, INCENP, MLPH, and KLK3 genes.

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INCENP

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