ASB9

Last update 08 May 2025

Basic Info

Synonyms

ankyrin repeat and SOCS box containing 9, Ankyrin repeat and SOCS box protein 9, ASB-9

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Introduction

Substrate-recognition component of a cullin-5-RING E3 ubiquitin-protein ligase complex (ECS complex, also named CRL5 complex), which mediates the ubiquitination and subsequent proteasomal degradation of target proteins (PubMed:25654263, PubMed:33268465). The ECS(ASB9) complex catalyzes ubiquitination of creatine kinases CKB and CKMT1A (PubMed:20302626, PubMed:22418839, PubMed:25654263, PubMed:33268465). Does not interact with the Elongin BC complex, likely to be a negative regulator of isoform 1.

100 Clinical Results associated with ASB9

100 Translational Medicine associated with ASB9

0 Patents (Medical) associated with ASB9

Literatures (Medical) associated with ASB9

01 Jan 2025·The American Journal of Human Genetics

Chromosome X-wide common variant association study in autism spectrum disorder

Article

Author: Scherer, Stephen W ; Salazar, Nelson Bautista ; Sun, Lei ; Roshandel, Delnaz ; Bandres-Ciga, Sara ; Alexandrova, Roumiana ; Trost, Brett ; Mendes, Marla ; Pellecchia, Giovanna ; Thiruvahindrapuram, Bhooma ; Lai, Meng-Chuan ; Bradley, Clarrisa A ; Anagnostou, Evdokia ; Rivera-Alfaro, Natalia ; Leal, Thiago Peixoto ; McKee, Ethan A ; Nalpathamkalam, Thomas ; Chen, Desmond Zeya ; Howe, Jennifer L ; Engchuan, Worrawat

Autism spectrum disorder (ASD) displays a notable male bias in prevalence. Research into rare (<0.1) genetic variants on the X chromosome has implicated over 20 genes in ASD pathogenesis, such as MECP2, DDX3X, and DMD. The "female protective effect" in ASD suggests that females may require a higher genetic burden to manifest symptoms similar to those in males, yet the mechanisms remain unclear. Despite technological advances in genomics, the complexity of the biological nature of sex chromosomes leaves them underrepresented in genome-wide studies. Here, we conducted an X-chromosome-wide association study (XWAS) using whole-genome sequencing data from 6,873 individuals with ASD (82% males) across Autism Speaks MSSNG, Simons Simplex Collection (SSC), and Simons Powering Autism Research (SPARK), alongside 8,981 population controls (43% males). We analyzed 418,652 X chromosome variants, identifying 59 associated with ASD (p values 7.9 × 10^-6 to 1.51 × 10^-5), surpassing Bonferroni-corrected thresholds. Key findings include significant regions on Xp22.2 (lead SNP rs12687599, p = 3.57 × 10^-7) harboring ASB9/ASB11 and another encompassing DDX53 and the PTCHD1-AS long non-coding RNA (lead SNP rs5926125, p = 9.47 × 10^-6). When mapping genes within 10 kb of the 59 most significantly associated SNPs, 91 genes were found, 17 of which yielded association with ASD (GRPR, AP1S2, DDX53, HDAC8, PCDH19, PTCHD1, PCDH11X, PTCHD1-AS, DMD, SYAP1, CNKSR2, GLRA2, OFD1, CDKL5, GPRASP2, NXF5, and SH3KBP1). FGF13 emerged as an X-linked ASD candidate gene, highlighted by sex-specific differences in minor allele frequencies. These results reveal significant insights into X chromosome biology in ASD, confirming and nominating genes and pathways for further investigation.

07 Jun 2023·Journal of animal science and biotechnology

CLOCK inhibits the proliferation of porcine ovarian granulosa cells by targeting ASB9.

Article

Author: Pang, Weijun ; Gao, Lei ; Zhou, Xiaoge ; Zhang, Lutong ; Song, Xiangrong ; Yuan, Huan ; Yang, Gongshe ; Chu, Guiyan ; Shi, Shengjie ; Huang, Liang

BACKGROUNDClock circadian regulator (CLOCK) is a core factor of the mammalian biological clock system in regulating female fertility and ovarian physiology. However, CLOCK's specific function and molecular mechanism in porcine granulosa cells (GCs) remain unclear. In this study, we focused on CLOCK's effects on GC proliferation.RESULTSCLOCK significantly inhibited cell proliferation in porcine GCs. CLOCK decreased the expression of cell cycle-related genes, including CCNB1, CCNE1, and CDK4 at the mRNA and protein levels. CDKN1A levels were upregulated by CLOCK. ASB9 is a newly-identified target of CLOCK that inhibits GC proliferation; CLOCK binds to the E-box element in the ASB9 promoter.CONCLUSIONSThese findings suggest that CLOCK inhibits the proliferation of porcine ovarian GCs by increasing ASB9 level.

01 Dec 2021·Molecular Reproduction and DevelopmentQ3 · BIOLOGY

Ankyrin‐repeat and SOCS box‐containing protein 9 (ASB9) regulates ovarian granulosa cells function and MAPK signaling

Q3 · BIOLOGY

Article

Author: Ndiaye, Kalidou ; Nosratpour, Soma

AbstractAnkyrin‐repeat and SOCS box‐containing proteins (ASB) interact with the elongin B‐C adapter via their SOCS box domain and with the cullin and ring box proteins to form E3 ubiquitin ligase complexes within the protein ubiquitination pathway. ASB9 in particular is a differentially expressed gene in ovulatory follicles (OFs) induced by the luteinizing hormone (LH) surge or hCG injection in ovarian granulosa cells (GC) while downregulated in growing dominant follicles. Although ASB9 has been involved in biological processes such as protein modification, the signaling network associated with ASB9 in GC is yet to be fully defined. We previously identified and reported ASB9 interactions and binding partners in GC including PAR1, TAOK1, and TNFAIP6/TSG6. Here, we further investigate ASB9 effects on target binding partners regulation and signaling in GC. CRISPR/Cas9‐induced inhibition of ASB9 revealed that ASB9 regulates PAR1, TAOK1, TNFAIP6 as well as genes associated with proliferation and cell cycle progression such as PCNA, CCND2, and CCNE2 while CCNA2 was not affected. Inhibition of ASB9 was also associated with increased GC number and decreased caspase3/7 activity, CASP3 expression, and BAX/BCL2 ratio. Furthermore, ASB9 induction in OF in vivo 24 h post‐hCG is concomitant with a significant decrease in phosphorylation levels of MAPK3/1 while pMAPK3/1 levels increased following ASB9 inhibition in GC in vitro. Together, these results provide strong evidence for ASB9 as a regulator of GC activity and function by modulating MAPK signaling likely through specific binding partners such as PAR1, therefore controlling GC proliferation and contributing to GC differentiation into luteal cells.

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ASB9

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