Ask about this productRelated genes to: CRLF1 Blocking Peptide
- Gene:
- CRLF1 NIH gene
- Name:
- cytokine receptor like factor 1
- Previous symbol:
- -
- Synonyms:
- CLF-1, CLF, CISS, CISS1
- Chromosome:
- 19p12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-26
- Date modifiied:
- 2018-04-23
Related products to: CRLF1 Blocking Peptide
Related articles to: CRLF1 Blocking Peptide
- Crisponi syndrome, also referred to as cold-induced sweating syndrome type 1, is an uncommon autosomal recessive disorder caused by mutations in the cytokine receptor-like factor 1 () gene. The disorder typically presents with distinctive craniofacial abnormalities, feeding impairment, stimulus-induced muscle spasms, and varying degrees of autonomic dysfunction. Neonates affected by this condition are particularly vulnerable to respiratory complications and infections, especially in the setting of prematurity. We report a case of a preterm male neonate born at 34 weeks of gestation to consanguineous parents, presenting with characteristic dysmorphic features and early-onset stimulus-induced spastic episodes. Initially suspected to have hypoxic-ischemic encephalopathy, the patient later developed severe respiratory distress and sepsis secondary to bilateral pneumonia. Laboratory findings showed progressive inflammatory markers, hematological abnormalities, and a positive blood culture for species. Retrospective assessment using the neonatal Sequential Organ Failure Assessment score yielded a score of 11, indicating severe organ dysfunction and high mortality risk. Whole exome sequencing confirmed a homozygous likely pathogenic variant in the gene, consistent with Crisponi syndrome. Despite intensive care management, the patient succumbed to multiorgan failure. This case highlights the diagnostic challenges in distinguishing neurological manifestations of Crisponi syndrome from hypoxic brain injury and underscores the high risk of severe infection in affected preterm neonates. Early genetic diagnosis and multidisciplinary management are critical for improving outcomes. - Source: PubMed
Publication date: 2026/05/11
Ravikumar DivyaSabina Garayeva - Cytokine-like receptor family 1 (CRLF1) has been implicated in tumor progression, yet its prognostic function and mechanistic actions in prostate cancer (PCa) remain elusive. This investigation sought to clarify the functional role, molecular mechanisms, and clinical relevance of CRLF1 in the progression of PCa. We conducted extensive bioinformatics analyses utilizing the protein interaction networks and the TCGA-PRAD dataset. CRLF1 and cartilage oligomeric matrix protein (COMP) expression were validated in clinical samples by qRT-PCR and Western blot (WB). Functional assessments, including Transwell invasion, flow cytometry, CCK-8, and wound healing, were conducted in vitro. An in vivo xenograft tumor model was used for further validation. Mechanistic investigations involved genetic perturbation (overexpression and inhibition) of CRLF1 and COMP. Compared to benign tissues, the levels of CRLF1 and COMP were markedly elevated in PCa tissues. Bioinformatics assessments illustrated a robust positive relationship between CRLF1 and COMP, suggesting COMP may function as a downstream mediator. In vitro and in vivo investigations illustrated that silencing CRLF1 significantly suppressed PCa cell growth, invasion, and tumor progression, while enhancing apoptosis. Importantly, suppressing COMP counteracted the cancer-promoting effects triggered by CRLF1 overexpression. At the mechanistic level, CRLF1 facilitates tumor progression by modulating COMP to activate the FAK/PI3K/AKT signaling cascade. Our outcomes demonstrate that CRLF1 promotes PCa progression by targeting COMP to stimulate the FAK/PI3K/AKT signaling axis. This newly identified CRLF1/COMP/FAK/PI3K/AKT pathway underscores CRLF1 as a potential biomarker and therapeutic target for PCa. - Source: PubMed
Publication date: 2026/04/28
Li ZhongzeWang JinrunXu LizheNing JinzhuoCheng Fan - Ovarian cancer (OV) remains the most lethal gynecological malignancy, owing to late‑stage diagnosis, high metastatic potential and limited therapeutic efficacy. Although the transcription factor zinc finger and BTB domain‑containing 7A (ZBTB7A) has been implicated in several types of cancer, its role in OV has not yet been systematically characterized. The present study comprehensively investigated the expression pattern, prognostic relevance, functional role and downstream mechanisms of ZBTB7A in OV progression. Multi‑cohort transcriptomic analyses across independent public datasets revealed consistent upregulation of ZBTB7A in OV tissues, and high expression predicted a significantly poor prognosis. Single‑cell RNA sequencing demonstrated that ZBTB7A‑high tumor cells were enriched in proliferative, migratory and epithelial‑mesenchymal transition‑related programs, accompanied by activation of oncogenic pathways such as Wnt/β‑catenin and Hippo‑YAP. Functional assays using overexpression and RNA interference demonstrated that ZBTB7A enhanced malignant phenotypes, including increased cell proliferation, DNA synthesis, clonogenic survival and migration. Further analyses identified cytokine receptor‑like factor 1 (CRLF1) as a key downstream effector of ZBTB7A. ZBTB7A overexpression elevated CRLF1 transcription, whereas CRLF1 knockdown abrogated ZBTB7A‑induced proliferation and migration, defining a functional ZBTB7A/CRLF1 oncogenic axis. Collectively, these findings establish ZBTB7A as an important transcriptional driver of OV aggressiveness and highlight the ZBTB7A/CRLF1 regulatory pathway as a potential prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/03/27
Hao XiaobaiChen Yu - Hypertrophic cardiomyopathy (HCM), the most common inherited cardiac disorder and a leading cause of sudden cardiac death in young adults, exhibits substantial genetic and clinical heterogeneity. Although sarcomere gene sequence variations account for a major proportion of HCM cases, nearly half of patients lack identifiable genetic defects, implying the involvement of undiscovered mechanisms that may converge on a common pathogenic pathway. However, a unified molecular basis underlying HCM pathogenesis remains undefined. - Source: PubMed
Publication date: 2026/03/16
Lin BowenWang JizhengLi CanWang ShuiyunShen MeitingHu LingjieChen LeiZhou FanhongLiu YiqiaoYang JianZhang MoWang DongXu GuoliangZhou BinSong LeiShi DanChen Yi-Han - Blood proteomic profiling may model vascular biological ageing with high precision. This study aimed to assess the association between blood pressure and proteomic vascular ageing, and its potential mediation role in the relationship between high blood pressure and incident cardiovascular events. - Source: PubMed
Kou MinghaoWang XuanMa HaoHeianza YorikoDorans KirstenBazzano LydiaQi Lu