Ask about this productRelated genes to: TCEAL3 antibody
- Gene:
- TCEAL3 NIH gene
- Name:
- transcription elongation factor A like 3
- Previous symbol:
- -
- Synonyms:
- MGC15737, WEX8
- Chromosome:
- Xq22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-16
- Date modifiied:
- 2016-02-15
Related products to: TCEAL3 antibody
Related articles to: TCEAL3 antibody
- Diabetic foot ulcer (DFU) is one of the most common and severe complications of diabetes, with vascular changes, neuropathy, and infections being the primary pathological mechanisms. Disulfidptosis, a recently identified form of programmed cell death, might be involved in the development of diabetic complications. This study aims to identify and validate potential disulfidptosis biomarkers associated with DFU through bioinformatics and machine learning analysis. - Source: PubMed
Publication date: 2025/10/08
Li JIeShi HongshuoCao Yemin - Intraductal papillary mucinous neoplasm (IPMN) is the most common type of pancreatic cyst often incidentally detected in asymptomatic patients. The current consensus guidelines, largely based on imaging features, have high sensitivity but low specificity in differentiating benign from malignant IPMNs, leading to unnecessary surgeries. Discovering biomarkers is thus warranted to improve the preoperative risk stratification of IPMN. Pancreatic cyst fluid samples were obtained from patients with pathologically confirmed low-grade (n = 73) or high-grade/invasive (n = 18) IPMN. Global proteome quantitation was performed using liquid chromatography-tandem mass spectrometry. Differentially expressed proteins (DEPs) between the two groups were analyzed using Wilcoxon rank-sum test. 152 upregulated and 74 downregulated DEPs were discovered by comparing low-grade IPMN with high-grade/invasive IPMN (all p < 0.05). The enriched upstream regulators of these DEPs included let-7, miR-122, IL15, and FLT1 (p = 6.76 × 10 - 5.97 × 10). Five discriminatory biomarkers with the largest LASSO coefficients and each with AUCs of >0.75 (FAHD2A, TCEAL3, TWF1, MMUT, and NTPCR) were identified. The combined five-protein model achieved a bootstrap-corrected AUC of 0.94. A combined analysis of TCGA and GTEx databases showed TWF1 overexpression in pancreatic cancer (p = 2.22 × 10) that was associated with poor prognosis (p = 0.0063). The present study identified several cyst fluid proteins (particularly TWF1) that are predictive of malignant pancreatic cyst lesions. If validated in other patient populations, these biomarkers may enhance the accuracy of the preoperative detection of high-risk IPMN and thereby improve patient outcomes. - Source: PubMed
Publication date: 2025/04/27
Liu ChunliangMosley AmberIrajizad EhsanYip-Schneider MicheleWu HuangbingSmith-Kinnaman Whitney RTran ThoaLong James PDo Kim-AnhFahrmann JohannesDeWitt John MHanash SamirSchmidt C MaxZhang Jianjun - An Xq22.2 region upstream of PLP1 has been proposed to underly a neurological disease trait when deleted in 46,XX females. Deletion mapping revealed that heterozygous deletions encompassing the smallest region of overlap (SRO) spanning six Xq22.2 genes (BEX3, RAB40A, TCEAL4, TCEAL3, TCEAL1, and MORF4L2) associate with an early-onset neurological disease trait (EONDT) consisting of hypotonia, intellectual disability, neurobehavioral abnormalities, and dysmorphic facial features. None of the genes within the SRO have been associated with monogenic disease in OMIM. Through local and international collaborations facilitated by GeneMatcher and Matchmaker Exchange, we have identified and herein report seven de novo variants involving TCEAL1 in seven unrelated families: three hemizygous truncating alleles; one hemizygous missense allele; one heterozygous TCEAL1 full gene deletion; one heterozygous contiguous deletion of TCEAL1, TCEAL3, and TCEAL4; and one heterozygous frameshift variant allele. Variants were identified through exome or genome sequencing with trio analysis or through chromosomal microarray. Comparison with previously reported Xq22 deletions encompassing TCEAL1 identified a more-defined syndrome consisting of hypotonia, abnormal gait, developmental delay/intellectual disability especially affecting expressive language, autistic-like behavior, and mildly dysmorphic facial features. Additional features include strabismus, refractive errors, variable nystagmus, gastroesophageal reflux, constipation, dysmotility, recurrent infections, seizures, and structural brain anomalies. An additional maternally inherited hemizygous missense allele of uncertain significance was identified in a male with hypertonia and spasticity without syndromic features. These data provide evidence that TCEAL1 loss of function causes a neurological rare disease trait involving significant neurological impairment with features overlapping the EONDT phenotype in females with the Xq22 deletion. - Source: PubMed
Publication date: 2022/11/10
Hijazi HadiaReis Linda MPehlivan DavutBernstein Jonathan AMuriello MichaelSyverson ErinBonner DevonEstiar Mehrdad AGan-Or ZivRouleau Guy ALyulcheva EkaterinaGreenhalgh LynnTessarech MarineColin EstelleGuichet AgnèsBonneau Dominiquevan Jaarsveld R HLachmeijer A M ARuaud LyseLevy JonathanTabet Anne-ClaudePloski RafalRydzanicz MałgorzataKępczyński ŁukaszPołatyńska KatarzynaLi YidanFatih Jawid MMarafi DanaRosenfeld Jill ACoban-Akdemir ZeynepBi WeiminGibbs Richard AHobson Grace MHunter Jill VCarvalho Claudia M BPosey Jennifer ESemina Elena VLupski James R - Projection neurons of the mammalian central nervous system (CNS) do not spontaneously regenerate axons which have been damaged by an injury or disease, often leaving patients with permanent disabilities that affect motor, cognitive, or sensory functions. Although several molecular targets which promote some extent of axon regeneration in animal models have been identified, the resulting recovery is very limited, and the molecular mechanisms underlying the axonal regenerative failure in the CNS are still poorly understood. One of the most studied targets for axon regeneration in the CNS is the mTOR pathway. A number of developmentally regulated genes also have been found to play a role in CNS axon regeneration. Here, we found that Transcriptional Elongation Factor A Like 3 (Tceal3), belonging to the Bex/Tceal transcriptional regulator family, which also modulates the mTOR pathway, is developmentally upregulated in retinal ganglion cell (RGCs) projection CNS neurons, and suppresses their capacity to regenerate axons after injury. - Source: PubMed
Publication date: 2021/09/21
Lukomska AgnieszkaKim JuhwanRheaume Bruce AXing JianHoyt AlexelaLecky EmmalynSteidl TylerTrakhtenberg Ephraim F - Heart failure (HF) is associated with pathological remodeling of the myocardium, including the initiation of fibrosis and scar formation by activated cardiac fibroblasts (CFs). Although early CF-dependent scar formation helps prevent cardiac rupture by maintaining the heart's structural integrity, ongoing deposition of the extracellular matrix in the remote and infarct regions can reduce tissue compliance, impair cardiac function, and accelerate progression to HF. In our study, we conducted mass spectrometry (MS) analysis to identify differentially altered proteins and signaling pathways between CFs isolated from 7 day sham and infarcted murine hearts. Surprisingly, CFs from both the remote and infarct regions of injured hearts had a wide number of similarly altered proteins and signaling pathways that were consistent with fibrosis and activation into pathological myofibroblasts. Specifically, proteins enriched in CFs isolated from MI hearts were involved in pathways pertaining to cell-cell and cell-matrix adhesion, chaperone-mediated protein folding, and collagen fibril organization. These results, together with principal component analyses, provided evidence of global CF activation postinjury. Interestingly, however, direct comparisons between CFs from the remote and infarct regions of injured hearts identified 15 differentially expressed proteins between MI remote and MI infarct CFs. Eleven of these proteins (, and ) were higher in MI infarct CFs, whereas four proteins (, and ) were higher in MI remote CFs. Collectively, our study shows that MI injury induced global changes to the CF proteome, with the magnitude of change reflecting their relative proximity to the site of injury. - Source: PubMed
Publication date: 2021/03/31
Shah HaisamHacker AlisonLangburt DylanDewar MichaelMcFadden Meghan JZhang HangjunKuzmanov UrosZhou Yu-QingHussain BilalEhsan FahadHinz BorisGramolini Anthony OHeximer Scott P