Ask about this productRelated genes to: CALB1 Blocking Peptide
- Gene:
- CALB1 NIH gene
- Name:
- calbindin 1
- Previous symbol:
- CALB
- Synonyms:
- -
- Chromosome:
- 8q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-11-09
Related products to: CALB1 Blocking Peptide
Related articles to: CALB1 Blocking Peptide
- Medial temporal lobe hyperexcitation or seizures originating from the hippocampus are frequently observed in Alzheimer's disease (AD) patients, contributing to accelerated cognitive decline. As the hippocampus is an early vulnerable area of tau pathology, the mechanisms by which abnormal tau aggregation promotes temporal lobe epilepsy (TLE) remain poorly understood. - Source: PubMed
Publication date: 2026/05/12
Gao YangTao XiaoqingWang YuyingWang YarongLi HuanYu YangTu MengqiLiu YanchaoZhou JieLi YuchenWei WeiWang XiaochuangZheng JieZhang YaoXu HaiboWang Jian-Zhi - Anticipating daily food availability is a conserved circadian behavior that persists even in animals lacking the suprachiasmatic nucleus, yet the neural substrates of this behavior remain poorly defined. Striatal dopamine signaling through D1 receptors promotes food anticipatory activity (FAA), but the dopaminergic neurons responsible are unknown. Here, we conditionally deleted () from genetically defined dopaminergic neuronal populations in mice. Broad deletion of in dopamine transporter-expressing neurons nearly abolished FAA, while viral restoration of in substantia nigra neurons was sufficient to rescue anticipatory locomotion. Surprisingly, deletion of from several large molecularly defined dopamine neuron populations had little effect on FAA. In contrast, deletion using , affecting a relatively small subset (25%) of substantia nigra dopamine neurons, produced a profound FAA deficit. Notably, these mice retained anticipatory food-seeking behavior but failed to express anticipatory locomotion. These findings identify a small Calbindin1 dopamine population that is required for the motor expression, but not the timekeeping, of food anticipation, revealing a genetic dissociation between circadian prediction and behavioral output. - Source: PubMed
Publication date: 2026/03/31
Villa Andrew PTrzeciak JacquelineWolfe DamienEhichioya David EFalkenstein JeffreyWong Justine TDimalanta LaurenKaiban WyattDhanoa JaskaranStevens GregoryGarcia FernandoScarpa LoriChalfoun ChrisZweifel Larry SAwatramani RajeshwarPalmiter Richard DDarvas MartinYamazaki ShinSteele Andrew D - The epigenetic modification N6-methyladenosine (mA) is critical for neurodevelopment. However, its interplay with histone modifications during cerebellar development remains poorly understood. Ythdf2 is a core mA reader that promotes selective degradation of methylated transcripts to shape gene expression dynamics. However, whether Ythdf2 also coordinates epitranscriptomic regulation with chromatin remodeling during cerebellar development is unknown. Here, we generated a Ythdf2 knockout (Ythdf2) mouse model and examined cerebellar development at embryonic day 13.5 (E13.5) and postnatal day 3 (P3). Ythdf2 mice developed overt cerebellar ataxia, manifested by tremors and abnormal gait. At the molecular level, loss of Ythdf2 disrupted neural progenitor maintenance and induced premature neuronal differentiation. The expression of progenitor markers, including Sox2, Nestin and Pax6 were markedly reduced, whereas markers of neuronal differentiation such as Tuj1 and Skor2 were increased. In contrast, genes associated with neuronal maturation, including Map2 and Calb1, and astrocytic marker Gfap were downregulated. m⁶A RIP seq analysis demonstrated that Ythdf2 caused a global reduction in m⁶A levels, with the differentially expressed m⁶A modified genes enriched for histone modification and chromatin stability. Furthermore, Ythdf2 loss suppressed transcriptional activity by altering H3K4me3 deposition, thereby reducing chromatin accessibility within neuronal developmental pathways. Co-immunoprecipitation revealed a specific interaction between YTHDF2 and the H3K4 methyltransferase SETD1B, but not CXXC1 or SETD1A, and Setd1b knockdown rescued the neural self-renewal and differentiation defects caused by Ythdf2 deletion. Together, these results establish a mechanistic link in which Ythdf2 connects mA-modified transcripts to Setd1b-mediated H3K4me3 deposition, thereby sustaining chromatin accessibility and transcriptional programs required for proper cerebellar development. - Source: PubMed
Publication date: 2026/04/03
Ren XiaolongJiang JingHu XiujuanZhang MingLi JinchengLu JiafengXia WenjuanDing ChenyueMeng QingxiaHuang Boxian - Short-chain fatty acids (SCFAs), metabolic products of the gut microbiota, are important regulators of intestinal homeostasis. SCFAs exert their effects through free fatty acid receptors (FFAR), which are located on enteroendocrine cells and enteric nerves. The actions of SCFAs include the regulation of motility. How SCFAs affect enteric neuronal activity and the regulation of colonic motility remains to be fully elucidated. - Source: PubMed
Wongkrasant PreedajitWallace Laurie ELe DavidMacNaughton Wallace KSharkey Keith A - The epithelial sodium channel (ENaC) is essential for sodium reabsorption and potassium homeostasis in the distal nephron, where its activity is controlled by mineralocorticoid signaling and downstream proteolytic processing of channel subunits. Although cleavage of the γ-ENaC subunit has been implicated in aldosterone-mediated sodium transport, the identity of mineralocorticoid receptor (MR)-regulated proteases responsible for this process remains uncertain. Here, we investigated the role of kallikrein-1 (encoded by ), a serine protease expressed in the connecting tubule and cortical collecting duct (CNT/CCD), as a mediator of ENaC activation. Using CRISPR/Cas9, we generated a conditional -floxed allele and established mice with CNT/CCD-specific deletion of by crossing with -Cre (CNT-). On a low-sodium, high-potassium diet, CNT-mice exhibited ∼85% less renal kallikrein-1 expression, yet maintained normal serum electrolytes, urinary potassium excretion, and aldosterone responses. Western blot analysis revealed significantly less cleavage of γ-ENaC and α-ENaC in CNT- kidneys, accompanied by more total NCC abundance. Despite impaired ENaC proteolysis, amiloride-sensitive sodium excretion was preserved, indicating intact ENaC function. These findings identify renal kallikrein-1 as a protease that contributes to ENaC subunit processing in vivo. However, the absence of overt sodium or potassium handling defects in CNT- mice suggests that kallikrein-1 deficiency is not sufficient to disrupt overall ENaC function, likely due to compensatory mechanisms from redundant proteolytic or nonproteolytic pathways. Together, our results refine the role of kallikrein-1 as a modulator, rather than a sole determinant, of ENaC activation and highlight the complexity of aldosterone-dependent sodium transport in the distal nephron. Using a novel connecting tubule/cortical collecting duct specific kallikrein-1 knockout model, we show that γ- and α-ENaC cleavage is impaired by loss of renal kallikrein-1, without major disturbances in sodium or potassium handling. These findings highlight redundancy among ENaC regulatory pathways and suggest that proteolytic cleavage of ENaC, although useful as an indicator of ENaC-mediated transport under physiological conditions, may not, in and of itself, play a major role in ENaC function. - Source: PubMed
Publication date: 2026/02/11
Curry Joshua NSu Xiao-TongWu QiMaeoka YujiroYang Chao-LingDelpire EricFenton Robert AWelling Paul AEllison David H