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At least 19 recordsLinked to original sources

PubMed1999

Effects of space flight on the immunohistochemical demonstration of connexin 26 and connexin 43 in the postpartum uterus of rats.

The effect of space flight in a National Aeronautics and Space Administration shuttle was studied in pregnant rats. Rats were launched on day 11 of gestation and recovered on day 20 of gestation. Pregnancy was allowed to proceed to term and rats delivered vaginally on days 22-23, although flight animals required more labour contractions to complete the delivery process. Pups were placed with foster dams and connexin 26 and 43 were examined in the uterus of flight animals approximately 3 h after delivery. Space flight did not affect uterine connexin 26, localized primarily in epithelial cells of the endometrium, but decreased connexin 43, the major gap junction protein in the myometrium. It is suggested that decreased connexin 43 alters synchronization and coordination of labour contractions, resulting in a requirement for more contractions to complete the delivery process.

Analysis of Variance↗

PubMed1997

Different changes in expression and function of connexin 26 and connexin 32 during DNA synthesis and redifferentiation in primary rat hepatocytes using a DMSO culture system.

In the present study, we determined in detail the changes of liver gap junctions, connexin 26 (Cx26), and connexin 32 (Cx32), during DNA synthesis and redifferentiation of hepatocytes in vitro. We used primary rat hepatocytes that expressed the liver gap junction proteins, which were cultured in the medium containing epidermal growth factor (EGF) with 2% dimethylsulfoxide (DMSO) and 10(-7) mol/L glucagon (a DMSO culture system), as we previously reported. In the present cultures, almost confluent hepatocytes cultured in the medium containing EGF with 2% DMSO and 10(-7) mol/L glucagon, underwent a nearly synchronous wave of DNA synthesis induced by the removal of 2% DMSO and 10(-7) mol/L glucagon, and the addition of 10 mmol/L nicotinamide, after which the DNA synthesis was completely re-inhibited by the re-addition of 2% DMSO and 10(-7) mol/L glucagon. During stimulation of DNA synthesis, both Cx26 and Cx32 messenger RNA (mRNAs) in hepatocytes transiently increased in the G1 phase and then markedly decreased before the onset of the S phase, while only Cx26 messenger RNA (mRNA) increased slightly in the S/M phase. Furthermore, before the onset of the S phase, a disappearance of both Cx26 and Cx32 immunoreactivities and gap junction plaques were observed. Gap junctional intercellular communication (GJIC), as measured by lucifer yellow, which indicated the function of Cx32, decreased markedly from before the onset of the S phase. GJIC measured by propidium iodide, which indicated the function of Cx26, decreased from before the onset of the S phase and then increased slightly in the S/M phase. During the re-inhibition after the stimulation of DNA synthesis, Cx32 mRNA, but not Cx26 mRNA, rapidly returned to the pretreatment control level. Cx32 immunoreactivity and gap junction plaques also recovered. However, the recovery of GJIC measured by lucifer yellow was later than that of Cx32 expression. These results indicated the different changes of expression and function of Cx26 and Cx32 in the hepatocytes during stimulation and re-inhibition of DNA synthesis. This culture system should be useful as a model in which to study liver gap junctions during hepatocyte growth and differentiation in vitro.

Actins↗

PubMed2004

Connexin 26 and connexin 30 mutations in children with nonsyndromic hearing loss.

OBJECTIVES/HYPOTHESIS: Mutations in the connexin 26 (Cx26) or gap junction beta 2 gene are the leading cause of hereditary nonsyndromic sensorineural hearing loss in Caucasians. The Cx26 coding region of 68 children with nonsyndromic sensorineural hearing loss was sequenced to determine the frequency and type of Cx26 mutations in this population. Screening was also performed for a common connexin 30 (Cx30) or gap junction beta 6 mutation (del [GJB6-D13S1830]). Children also underwent audiological testing to determine whether any correlation exists between Cx26 mutations and severity of hearing loss. STUDY DESIGN: In all, 68 children with nonsyndromic sensorineural hearing loss were screened for Cx26 and Cx30 mutations by polymerase chain reaction and direct sequencing. METHODS: Genomic DNA was amplified by polymerase chain reaction using primers that flank the entire Cx26 coding region. Screening for the 342-kb Cx30 deletion was performed using primers that amplified the breakpoint junction of the deletion. The amplicons were then sequenced in both directions and analyzed for mutations. Audiometric testing, including pure-tone audiometry and auditory evoked brainstem response, was also performed to determine the degree of hearing loss. RESULTS: Twenty-seven of 68 children tested had mutations in Cx26 with 35delG being the most prevalent. Ten additional Cx26 mutations were detected including a novel compound heterozygote. Two children were heterozygous for the Cx30 del (GJB6-D13S1830) mutation. CONCLUSION: Cx26 and Cx30 mutations were present in 41.2% of children tested in the study population. Audiometric data supported previous studies demonstrating a greater degree of hearing loss in subjects who are homozygous for the 35delG mutation.

Adolescent↗

PubMed1998

Expression of gap junction proteins connexin 26 and connexin 43 in normal human breast and in breast tumours.

Gap junctional intercellular communication (GJIC) has been proposed as a cellular mechanism for tumour suppression and there is experimental evidence in support of this. If aberrant GJIC contributes to the formation of human breast tumours, one might expect that the connexins (gap junction proteins) expressed by epithelial cells in normal human breast would be down-regulated in tumour epithelial cells, or that tumour cells might show aberrant expression of other connexin family members. This study examines the immunocytochemical expression of connexins 26 (Cx26) and 43 (Cx43) in normal human breast, 11 benign breast lesions, two special-type carcinomas, and 27 invasive carcinomas of no special histological type (NST). Cx26 generally was not expressed at detectable level in normal human breast, but punctate Cx43 immunostaining of the myoepithelial cells was found. Cx43 staining of the myoepithelium was also a feature of the benign lesions and ductal carcinoma in situ (DCIS). In general, the epithelial cells of benign lesions failed to stain for either connexin. Similarly, a lobular carcinoma did not express Cx26 or Cx43, but there was punctate Cx43 in the epithelial cells of a mucoid carcinoma. Cx26 was up-regulated in the carcinoma cells of 15 of the 27 invasive NST carcinomas, although the staining was usually cytoplasmic and heterogeneous. Cx43 was expressed by stromal cells, possibly myofibroblasts, in all NST carcinomas. Furthermore, there was heterogeneous Cx43 expression in the carcinoma cells of 14 of the 27 NST carcinomas and the staining was often intercellular and punctate, characteristic of functional connexins. Up-regulated of Cx26 and/or Cx43 in the carcinoma cells of over two-thirds of invasive lesions of NST is not necessarily inconsistent with a tumour suppressor role for GJIC. However, the role of gap junctions in the formation and progression of solid human tumours is likely to be more complex than indicated from experimental systems.

Breast↗

PubMed2006

Expression patterns of connexin 26 and connexin 43 mRNA in canine benign and malignant mammary tumours.

The expression patterns of connexin (Cx) genes, encoding gap junctional proteins, are tissue- and cell-specific and, as their expression is mostly suppressed during carcinogenic processes, they are appropriate for monitoring tumour development. In this study, using reverse transcriptase-coupled polymerase chain reaction (RT-PCR), the expression of Cx mRNAs was examined in seven normal canine mammary glands and in 31 mammary gland tumour samples. Cx26 and Cx43 gene expression was studied in all normal tissues using specific Cx26 and Cx43 primers. When the expression patterns of Cx26 and Cx43 genes were analyzed in several types of canine mammary gland tumours, it was noted that it was the loss of Cx26 expression rather than the occurrence of Cx43 expression that was associated with malignancy. These results suggest that Cx26 plays an important role in tumourigenesis of canine mammary gland.

Animals↗

PubMed2006

Expression of the gap junction proteins connexin 26 and connexin 43 in human middle ear cholesteatoma.

CONCLUSION: The results of this study showed upregulated expression and a change in localization of both connexin 43 (Cx43) and Cx26 in human middle ear cholesteatoma compared to those in normal retroauricular skins (RASs) and ear canal skins (ECSs). This suggests that perturbations of intercellular communication through gap junctions may be associated with the pathology of human cholesteatomas. OBJECTIVE: Cholesteatomas in the middle ear require intercellular signal exchange through gap junctions as well as intracellular signal pathways for the hyperproliferation and differentiation of epithelial cells. Cx is a gap junction protein involved in intercellular communication. The objective of this study was to analyze the expression and possible roles of Cx43 and Cx26 in human cholesteatoma compared to normal epithelium. MATERIAL AND METHODS: Ten RASs, 10 ECSs and 10 cholesteatomas were obtained during middle ear operations. Immunohistochemical staining, Western blotting and reverse transcriptase polymerase chain reaction (RT-PCR) were used to detect Cx43 and Cx26. The expression patterns of Cx43 and Cx26 were also compared with that of the proliferation marker Ki67. RESULTS: In human cholesteatomas, Cx43 was expressed in whole suprabasal layers, except in the basal layer, and Cx26 was usually expressed in the suprabasal and basal layers. However, normal RASs showed weak expression of Cx43 in the upper spinosal and granular layers (with no expression in the basal layers) and restricted localization of Cx26 in the basal layer. The expression of Cx43 and Cx26 in ECSs was weak but showed similar patterns to that of cholesteatoma. RT-PCR and Western blotting showed that the expression of Cx43 and Cx26 was higher in cholesteatoma than in RASs. Epithelial cells expressing Cx43 and Cx26 in cholesteatoma were not exactly identical to Ki67-expressing cells on immunohistochemical staining.

Blotting, Western↗

PubMed2005

Hearing impairment in Dutch patients with connexin 26 (GJB2) and connexin 30 (GJB6) mutations.

OBJECTIVE: Despite the identification of mutations in the connexin 26 (GJB2) gene as the most common cause of recessive nonsyndromic hearing loss, the pattern of hearing impairment with these mutations remains inconsistent. Recently a deletion encompassing the GJB6 gene was identified and hypothesized to also contribute to hearing loss. We hereby describe the hearing impairment in Dutch patients with biallelic connexin 26 (GJB2) and GJB2+connexin 30 (GJB6) mutations. METHODS: The audiograms of patients who were screened for GJB2 and GJB6 mutations were analysed retrospectively. Standard statistical testing was done for symmetry and shape, while repeated measurement analysis was used to assess the relation between mutation and severity. Progression was also studied via linear regression analysis. RESULTS: Of 222 hearing-impaired individuals, 35 exhibited sequence variations; of these 19 had audiograms for study. Hearing loss in patients with biallelic "radical" (i.e. deletions, nonsense and splice site) mutations was significantly worse than in the wild type and heterozygotes (SAS proc GENMOD, p=0.013). The presence of at least one missense mutation in compound heterozygotes tends to lead to better hearing thresholds compared to biallelic radical mutations (p=0.08). One patient with the [35delG]+[del(GJB6-D13S1830)] genotype was severely impaired. Non-progressive hearing impairment was demonstrated in five 35delG homozygotes in individual longitudinal analyses. However a patient with the [299A>C]+[416G>A] genotype showed significant threshold progression in the lower frequencies. Findings on asymmetry and shape were inconclusive. CONCLUSIONS: Our data support the hypothesis that severity is a function of genotype and its effect on the amino acid sequence. A bigger cohort is required to establish non-progressivity more definitively.

Adolescent↗

PubMed2005

Ethnicity and mutations in GJB2 (connexin 26) and GJB6 (connexin 30) in a multi-cultural Canadian paediatric Cochlear Implant Program.

OBJECTIVE: To determine the relationship between ethnicity and mutations in the GJB2 and GJB6 genes in multi-cultural patients enrolled in a Canadian paediatric Cochlear Implant Program. METHODS: Blood was analyzed from 65 paediatric cochlear implant users by direct sequencing of the coding region and intron/exon boundaries of the GBJ2 gene. Individuals heterozygous for one mutation in GJB2 or in whom mutations in GJB2 were not detected were analyzed for the common 342 kb deletion mutation D13S1830 in the GJB6 gene. Information regarding ethnicity of patients' families was obtained from patient records and/or interview. RESULTS: GJB2 mutations were found in 36.9% of paediatric cochlear implant users tested. Nine different GJB2 mutations were identified among individuals from 14 different countries of origin. Seventy-eight percent of all identified pathogenic GJB2 mutations were 35delG. Biallelic GJB2 mutations were found in 16 cochlear implant users (66.7% of GJB2 mutations). Three novel GJB2 sequence changes were identified: (1) a missense mutation T107C (L36P) in an individual of African decent; (2) a missense mutation G475T (D159Y) in an individual of Caribbean decent; (3) a regulatory region change 1-34C to T in an individual of African decent. GJB6-D13S1830 mutations were not found in any of the patients tested. Individuals of African, Caribbean and East Indian decent had different GJB2 mutations than the remainder of individuals tested. Patients of Asian, Italian, Spanish, Polish and Armenian decent were not found to carry mutations in GJB2 or the common GJB6-D13S1830 mutation. CONCLUSIONS: This study represents the largest number of biallelic GJB2 mutations isolated in a group of paediatric cochlear implant users to date. Numerous and diverse GJB2 mutations were found in this multi-cultural group of children. Even though GJB2 mutations have been widely reported in the literature, this discussion represents the first report of GJB2 mutations in a multi-ethnic population (Canadian), as compared with previous studies that investigated fairly homogeneous populations. The diversity of GJB2 mutations identified reinforces the importance of testing for changes in GJB2 by direct sequencing of the entire coding region rather than testing only for common mutations.

Canada↗

PubMed2001

Reduction of malignant phenotype of HEPG2 cell is associated with the expression of connexin 26 but not connexin 32.

Connexin (Cx) genes have a negative growth effect on tumour cells with certain specificity. However, it is not clear whether each Cx gene can act similarly in growth control. Hepatocytes normally express Cx26 and Cx32 as their major gap junction genes, but HepG2 cells, a hepatoma cell line, are deficient in gap junctional intercellular communication (GJIC) based on the down-regulation of Cx26 and aberrant localization of Cx32. In this study, we showed that some of the expressed Cx26 protein in HepG2 cells localized in the plasma membrane and contributed to recovery of GJIC, while the Cx32 protein remained localized in the cytoplasm. The Cx26-transfected clones showed a significantly slower growth in vivo as well as in vitro and reduced anchorage-independent growth ability compared with a mock-transfected clone. Cx26-transfected cells had more regular cell layers due to the re-establishment of the E-cadherin cell adhesion complex. E-cadherin expression following Cx26 transfection was induced. Cx26 expression simultaneously brought E-cadherin and beta-catenin proteins into the plasma membrane without any change in the expression level of beta-catenin protein. These results suggest that the expression of Cx26 contributes to negative growth control of HepG2 cells and the morphological change through the induction of E-cadherin and subsequent formation of cell adhesion complex.

Animals↗

PubMedDate not supplied

Frequency and distribution of GJB2 (connexin 26) and GJB6 (connexin 30) mutations in a large North American repository of deaf probands.

PURPOSE: Profound hearing loss occurs with a frequency of 1 in 1000 live births, half of which is genetic in etiology. The past decade has witnessed rapid advances in determining the pathogenesis of both syndromic and nonsyndromic deafness. The most significant clinical finding to date has been the discovery that mutations of GJB2 at the DFNB1 locus are the major cause of profound prelingual deafness in many countries. 1 More recently, GJB2 mutations have been shown to cause deafness when present with a deletion of the GJB6 gene. We report on the prevalence of GJB2 and GJB6 mutations in a large North American Repository of DNA from deaf probands and document the profound effects of familial ethnicity and parental mating types on the frequency of these mutations in the population. METHODS: Deaf probands were ascertained through the Annual Survey of Deaf and Hard of Hearing Children and Youth, conducted at the Research Institute of Gallaudet University. Educational, etiologic, and audiologic information was collected after obtaining informed consent. DNA studies were performed for the GJB2 and GJB6 loci by sequencing and PCR methods. RESULTS: GJB2 mutations accounted for 22.2% of deafness in the overall sample but differed significantly among Asians, African-Americans and Hispanics and for probands from deaf by deaf and deaf by hearing matings, as well as probands from simplex and multiplex sibships of hearing parents. In our sample, the overall incidence of GJB2/GJB6 deafness was 2.57%. CONCLUSION: GJB2 mutations account for a large proportion of deafness in the US, with certain mutations having a high ethnic predilection. Heterozygotes at the GJB2 locus should be screened for the GJB6 deletion as a cause of deafness. Molecular testing for GJB2 and GJB6 should be offered to all patients with nonsyndromic hearing loss.

Alleles↗

PubMed2004

Longitudinal phenotypic analysis in patients with connexin 26 (GJB2) (DFNB1) and connexin 30 (GJB6) mutations.

In 15 Belgian subjects with prelingual sensorineural hearing impairment, the connexin 26 (GJB2) gene and the connexin 30 (GJB6) gene were analyzed for the presence of the 35delG mutation and the delta(GJB6-D13S1830) deletion first described by del Castillo et al in 2002. Seven patients were found to be homozygous for the 35delG mutation; 7 were combined heterozygotes for the 35delG mutation and the GJB6 deletion. In 11 subjects, phenotype and genotype were correlated. Significant, transient progression, in the range of 1.7 to 2.7 dB/y, was only found in 2 patients in the first part of the second decade of life. Hearing impairment was otherwise stable, with mean thresholds of 75, 90, and 100 dB at 0.125, 0.25, and 0.5 kHz, respectively, and 100 dB or higher at 1 to 4 kHz. There was no significant difference in hearing impairment between the patients with the homozygous 35delG mutation in GJB2 and those who are heterozygous for both the 35delG mutation and the deletion encompassing part of GJB6.

Adolescent↗

PubMed2000

The M34T allele variant of connexin 26.

GJB2 encodes the protein Connexin 26, one of the building blocks of gap junctions. Each Connexin 26 molecule can oligomerize with five other connexins to form a connexon; two connexons, in turn, can form a gap junction. Because mutations in GJB2 are the most common cause of congenital severe-to-profound autosomal recessive nonsyndromic hearing loss, the effect of the Connexin 26 allele variants on this dynamic 'construction' process and the function of any gap junctions that do form is particularly germane. One of the more controversial allele variants, M34T, has been hypothesized to cause autosomal dominant nonsyndromic hearing loss. In this paper, we present clinical and genotypic data that refutes this hypothesis and suggests that the effect of the M34T allele variant may be dependent on the mutations segregating in the opposing allele.

Alleles↗

PubMed2003

Connexin 26 is abnormally expressed in bladder cancer.

PURPOSE: Connexin 26 is the major gap junction protein in urothelial and mammary epithelial cells, and a putative tumor suppressor gene. We evaluated connexin 26 expression in normal urothelium and in bladder cancer. MATERIALS AND METHODS: A total of 40 formalin fixed, paraffin embedded bladder tumors and 5 normal urothelial specimens were analyzed by immunohistochemistry. Two observers visually scored connexin 26 expression in these specimens. RESULTS: Normal urothelium expressed connexin 26 in a punctate staining pattern with limited expression in the basal layer. Decreased connexin 26 expression was observed in 28 of 40 tumors (70%). Connexin 26 was diffusely expressed in 5 of 18 low grade, noninvasive tumors (28%), whereas loss of expression was observed in heterogeneous (30% to 70% positive staining) or extensive (less than 30% positive staining) fashion in 8 (44%) and 5 (28%), respectively. Seven of 22 high grade or invasive tumors (32%) showed diffuse connexin 26 expression, whereas expression was decreased in a heterogeneous or extensive pattern in 9 (41%) and 6 (27%), respectively. Intracytoplasmic localization of connexin 26 was also observed. CONCLUSIONS: Expression of connexin 26 is altered in bladder cancer. These aberrant patterns of connexin 26 expression may contribute to the malignant phenotype of this disease.

Carcinoma, Transitional Cell↗

PubMed1999

New Regulatory Sequence of Human Connexin 26 Gene.

Human connexin 26 gene (Cx26) has been considered a candidate suppressor gene in mammary epithelial cells. To explain regulatory mechanism of the Cx26, a DNase-1 hypersensitive 1.6 kb fragment upstream of the 5'-terminus of the gene was sequenced and assayed with CAT reporter system. The results showed that the 1.6 kb sequence had powerful promoter activity. The fragment contains two GT boxes (centering at -6158 and -6213 bp), and a TATA-less TTAAAA box (-6237/-6232 bp) which is the new promoter region of human Cx26.

Journal Article↗

PubMed2002

[From gene to disease: deafness and connexin 26].

Deafness is genetically heterogeneous, yet it is estimated that approximately half of the heritable cases of autosomal recessive deafness are caused by mutations in the gene coding for connexin 26. Connexin 26 is thought to have an essential role in the transport of potassium ions back to the endolymph of the inner ear after sound stimulation.

Connexin 26↗

PubMed2003

Targeted epidermal expression of mutant Connexin 26(D66H) mimics true Vohwinkel syndrome and provides a model for the pathogenesis of dominant connexin disorders.

To investigate the role of connexins in dominantly inherited skin disease, transgenic mice were produced which expressed mutant connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10 promoter, exclusively in the suprabasal epidermis (the cells in which Connexin 26 is up-regulated in epidermal hyperproliferative states). From soon after birth, the mice exhibited a keratoderma similar to that in humans carrying the Connexin 26(D66H) mutation (true Vohwinkel syndrome). Transgene expression was associated with loss of Connexin 26 and Connexin 30 from epidermal keratinocyte intercellular junctions and accumulation in cytoplasm. Light and electron microscopy showed marked thickening of the epidermal cornified layers and increased epidermal TUNEL staining, indicative of premature keratinocyte programmed cell death. The K10Connexin 26(D66H) mouse may provide a valuable model to study the role of gap-junctional intercellular communication in epidermal differentiation. Similarities in phenotype between individuals (man and mouse) carrying Connexin 26(D66H) and those carrying insertional mutants of Loricrin, a major cornified envelope protein of the epidermis, suggest a possible link between connexin function and cornified envelope formation.

Animals↗

PubMed2000

A connexin 26 mutation causes a syndrome of sensorineural hearing loss and palmoplantar hyperkeratosis (MIM 148350).

We report a missense mutation in the connexin 26 gene (GJB2) in a family with an autosomal dominant syndrome of hearing loss and hyperkeratosis. The affected family members have high frequency, slowly progressive, bilateral, sensorineural hearing loss and palmoplantar hyperkeratosis. The mutation causes an amino acid substitution (G59A), which may disrupt a reverse turn in the first extracellular loop of connexin 26. Connexin 26 mutations have been reported in syndromes of deafness and palmoplantar keratoderma. These data provide additional evidence for the role of connexin 26 in syndromes of this type.

Amino Acid Substitution↗

PubMed1994

The topological structure of connexin 26 and its distribution compared to connexin 32 in hepatic gap junctions.

Of the gap junction proteins characterized to date, Cx26 is unique in that it is usually expressed in conjunction with other members of the family, typically Cx32 (liver [Nicholson et al., Nature 329:732-734, 1987], pancreas, kidney, and stomach [J.-T. Zhang, B.J. Nicholson, J. Cell Biol. 109:3391-3410, 1989]), or Cx43 (leptomeninges [D.C. Spray et al., Brain Res. 568:1-14, 1991] and pineal gland [J.C. Sáez et al., Brain Res. 568:265-275, 1991]). We have used specific antisera both to investigate the distribution of Cx32 and Cx26 in isolated liver gap junctions, and empirically establish the topological model of Cx26 suggested by its sequence and analogy to other connexins. Antipeptide antisera were prepared to four of the five hydrophilic domains which flank the four putative transmembrane spanning regions of Cx26. Antibodies to N-terminal residues 1-17 (alpha Cx26-N), to residues 101-119 in the putative cytoplasmic loop (alpha Cx26-CL), and to C-terminal residues 210-226 (alpha Cx26-C) were all specific for Cx26. An antibody to residues 166-185 between hydrophobic domains 3 and 4 of Cx32 had affinity for both Cx26 and Cx32 (alpha Cx32/26-E2). The antigenic sites Cx26-N, -CL and -C were each demonstrated to be cytoplasmically disposed, although the latter was conformationally hidden prior to partial proteolysis. The antigenic site for alpha Cx32/26-E2 was only accessible after exposure of the extracellular face by separation of the junctional membranes in 8 M urea, pH 12.3. This treatment also served to reveal the region between residues 45 and 66 to Asp-N protease. The topology thus demonstrated for Cx26 is consistent with that deduced for other connexins (i.e., Cx32 and Cx43). Comparison of immunogold decorated gap junctions reacted with antibodies specific to Cx26 (alpha Cx26-N and -CL), or to Cx32 [alpha Cx32-CL], indicates that these connexins do not aggregate in subdomains within a junction, at least within the resolution provided by the labeling density (one antibody per 15-22 connexons). Although the presence of both connexins within a single channel could not be distinguished, possible interactions between channels is discussed.

Amino Acid Sequence↗